Page 153 - Coronary hemodynamics in acute myocardial infarction - Matthijs Bax

Time course of coronary flow capacity in STEMI
Introduction
Primary percutaneous coronary intervention (PCI) is considered the cornerstone for treating ST-segment elevation myocardial infarction (STEMI), and the implementation of dedicated revascularization networks has resulted in a remarkable decline in cardiac morbidity and mortality.1 Despite these advancements, a significant proportion of patients have a poor outcome, which is attributed to changes in the microvascular function and integrity due to the ischaemic event.2 It is increasingly recognized that the impact of the acute ischaemic event on the functional and structural integrity of the microcirculation may yield opportunities to further enhance clinical outcomes in STEMI patients.3
Coronary flow reserve (CFR) is a well-validated index that assesses the contribution of obstructive, diffuse and microcirculatory involvement to coronary flow impairment in ischaemic heart disease.4–6 In the past decades it has been extensively used to elucidate the role of microvascular dysfunction for the prognosis of myocardial infarction. However, assessing the coronary microcirculation solely by means of CFR is inherently cumbersome in STEMI patients, since residual effects of the ischaemic events and changes in (regional) cardiac workload may influence resting or hyperaemic flow and thereby obscure microvascular function assessment by CFR values.7
Recently the coronary flow capacity (CFC) concept has been validated as a
cross modality platform for the diagnosis, prognosis and risk-stratification in 9 ischaemic heart disease.7,8 It integrates both the coronary vasodilatory reserve
as well as maximal achievable flow, thereby providing comprehensive insight
into coronary haemodynamics.9 Accordingly, CFC was documented to be less
prone to alterations in systemic haemodynamics.10 In the present study we
aimed to document the impact of STEMI on CFC in 1) the ischaemic region of
the myocardium and 2) in myocardial territories remote from the infarction at
baseline, one-week and six-month follow-up.
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