Page 160 - Coronary hemodynamics in acute myocardial infarction - Matthijs Bax
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Chapter 9
Discussion
The present study is one of the first to document the impact of STEMI on myocardial perfusion using the validated CFC framework to comprehensively assess the consequences of focal obstructive, diffuse and microcirculatory causes of myocardial blood flow impairment. We have previously reported that microvascular function assessed by Doppler flow velocity is altered in the setting of STEMI, even in non-ischaemic regions at distance from the infarcted myocardial tissue and the independent association with long-term fatal cardiac events.
We observed a trend in infarct size for both the culprit vessel post PCI as well as the non-culprit vessel across CFC groups. In addition, an increase in time to reperfusion was associated with worsening of CFC determined after primary PCI in the both the culprit and the non-culprit vessel. CFC at the different time points resulted from an alternating contribution of the individual components that determine CFC group allocation; CFR, hAPV and bAPV. Of note, bAPV showed a significant trend across culprit vessel CFC groups after primary PCI and at one-week and six-month follow-up, but did not differ between groups in the non-culprit vessel.
CFC in the acute setting
First derived from positron emission tomography, the CFC concept integrates CFR with maximal hyperaemic flow velocity.7,9,14 It thereby captures all components of coronary flow physiology and provides a comprehensive tool to depict myocardial blood flow impairment due to a combination of obstructive, diffuse and microcirculatory involvement of the coronary vasculature. Hence, in the absence of epicardial disease the CFC concept provides insights into the microvascular function. In addition, it has been shown to provide an improvement in risk discrimination for adverse clinical outcomes compared with CFR alone.9
This concept is of particular interest when assessing microvascular function in the acute setting of STEMI, where mechanical and neurohumoral factors can have an effect on both resting and hyperaemic coronary flow,11 resulting in prolonged activation of the sympathetic nervous system,15,16 subsequently inducing a vasoconstrictive response of the coronary resistance vessels by
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