Page 143 - Coronary hemodynamics in acute myocardial infarction - Matthijs Bax

Elevated glucose levels impact microvascular function in STEMI
changes in response to the infarction, plays a distinct role in the pan-myocardial microvascular dysfunction observed in the acute setting of first anterior STEMI.
We found no association between microvascular function and admission glucose levels in the IRA. The influence of admission glucose levels on the parameters of microvascular function was likely eclipsed by other physiological processes that alter microvascular function in the IRA during the acute setting of STEMI.
Microvascular function following STEMI: novelty of the present findings
Microvascular function assessed by Doppler flow velocity is known to be
altered in the setting of STEMI, even in non-ischaemic regions at distance
from the infarcted myocardium.4 We previously reported that microvascular dysfunction in these regions is expressed in an impairment of reference vessel
CFVR, which is independently associated with long-term fatal cardiac events.11
We showed that the acute impairment of reference vessel CFVR in the setting
of STEMI originates from a combination of decreased hAPV in the presence
of increased HMR, and increased bAPV in the presence of decreased BMR.
It has been hypothesised that a combination of mechanical and metabolic alterations due to the acute ischaemic event is responsible for the overall
flow impairment at a distance of the infarcted myocardium. The increase
in HMR leading to impairment of hyperaemic flow is generally attributed to 8 neurohumoral overactivation.5 A reduced BMR leading to an increased resting
coronary flow may underlie a mechanical as well as a metabolic origin, which is yet to be elucidated. Our present results attribute at least part of the decrease in BMR, and the resulting increase in basal flow velocity, to metabolic changes in the setting of acute STEMI reflected in hyperglycaemia.
Glucose and insulin mediated microvascular dysfunction
Increased glucose levels are frequently observed in non-diabetic patients presenting with acute myocardial infarction. It reflects the conjoined effects of many interrelated stress mechanisms that influence glucose homeostasis secondary to the acute ischaemic event.7,16 Relative insulin resistance is proposed as one of the contributing mechanisms, caused by antagonising effects of stress mediators that impair insulin-regulated glucose uptake.17,18 Concomitantly, insulin plays an important role as a mediator in normal myocardial and systemic
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