Page 128 - Coronary hemodynamics in acute myocardial infarction - Matthijs Bax

Chapter 7
to understand these findings and implications, it is important to understand the differences between both indices. As shown in Table 2, baseline average peak velocity (APV) is probably increased due to compensatory vasodilatation, and the hyperaemic APV decreased probably secondary to microembolization. Since myocardial infarction affects both the baseline and hyperaemic coronary flow, both these effects are taken into account by the CFR, whereas the HMRI does not consider a baseline coronary flow. This observation is in accordance with previous studies. This increase in baseline peak flow velocity has been described as being a result of coronary autoregulation17,18. This is of importance as it facilitates the compensatory vasodilatation of the coronary resistance vessels in order to maintain stable resting coronary blood flow in the distal myocardium19.
We also assessed the temporal evolution of microvascular dysfunction, as measured by the delta CFR and HMRI between baseline and four months. In the large infarct size group, this observed improvement of CFR and decrease in HMRI were both associated with recovery of LVEF. In the smaller infarct size group this association was not observed. Our findings are concordant with the studies by Suryapranata et al15 and Sezer et al20, and extend on their findings. In the first study, an increase in flow reserve documented before hospital discharge was associated with a significant improvement in global and regional LVF15. In the Suryapranata et al study, improvement in CFR in the total population was associated with a decreased infarct size on single-photon emission computed tomography and improved LVEF on echocardiography.
Dysfunction of the coronary microvasculature has also been associated with the occurrence of clinical endpoints, including heart failure and cardiac mortality21-23. Furber at al assessed whether an impaired microvascular perfusion in the IRA, as measured by a short diastolic deceleration time, is predictive of cardiac events within four years21. In addition to age and time to PPCI ≥6 hours, impaired microvascular perfusion was found to be an independent predictor, particularly for the occurrence of heart failure. Also, an impaired CFR in the reference vessel in STEMI patients has been independently associated with an increased cardiac mortality at 10 years23. These clinical implications of microvascular dysfunction following STEMI have fueled studies on therapeutic strategies aimed at protecting the microvasculature24.
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