Page 89 - Coronary hemodynamics in acute myocardial infarction - Matthijs Bax

Coronary microvascular function and long-term mortality
and as an isolated increase in baseline APV in the reference vessel, resulting in
a lower CFVR in both territories.37 Third, neurohumoral activation in response
to the acute ischemic event interferes with the reactivity of the coronary
resistance vessels in the infarct-related as well as in remote regions. The rigorous
and persistent activation of the sympathetic nervous system38,39 results in
activation of coronary vascular α-adrenoceptors by neuronal and humoral cathecholamines,40 and induces a paradoxical vasoconstriction in times of
increased myocardial oxygen demand.41 Although metabolic vasodilation
prevails in such a situation, α-adrenergic vasoconstriction competes, resulting
in a decrease in hyperemic flow velocity, limiting CFVR throughout the
heart.42,43 Finally, impaired reference vessel CFVR, associated with a low baseline microvascular resistance, was shown to be of important prognostic value in
patients with stable coronary artery disease, in the absence of mechanical 5 myocardial dysfunction, and in the absence of an acute ischemic event.44 This
finding indicates that pre-existent microvascular dysfunction may play an important role in long-term clinical outcome.
Overall, mechanical factors induced by the acute ischemic event, as well as pre-existent microvascular alterations are primarily expressed as an increase in baseline flow velocity. Neurohumoral activation, however, results in an increase in reference vessel hyperemic microvascular resistance, resulting in a decrease in maximal hyperemic flow velocity. Both causes may thereby result in an impaired reference vessel CFVR.
Implications for the Present Study
We observed that an impaired reference vessel CFVR at the time of STEMI results predominantly from a low APV during the hyperemic response to an intracoronary bolus of adenosine, together with a less pronounced increase in baseline APV (Table 3).20 Because compensatory hyperkinesis in the remote regions is associated with a predominant increase in baseline flow velocity,28,32 compensatory hyperkinesis as the sole cause for the impaired reference vessel CFVR is unlikely. Additionally, although LVEDP was not measured in the present study, our study excluded patients with Killip class >2, and the study population consisted of patients in a hemodynamically stable state without known structural heart disease, in whom increase in LVEDP can be expected to be limited. Nonetheless, stiffening of the myocardium because
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