Coronary Microcirculation Downstream Non-Infarct-Related Arteries in the Subacute Phase of Myocardial Infarction: Implications for Physiology-Guided Revascularization

Abstract

Background Concerns exist about reliability of pressure-wire-guided coronary revascularization of non-infarct-related arteries (non- IRA ). We investigated whether physiological assessment of non- IRA during the subacute phase of myocardial infarction might be flawed by microcirculatory dysfunction. Methods and Results We analyzed non- IRA that underwent fractional flow reserve, coronary flow reserve, and the index of microcirculatory resistance assessment. Microcirculation and hyperemic response were evaluated in 49 acute myocardial infarction patients (59 non- IRA ) and compared with a matched control group of 46 stable angina ( SA ) patients (59 vessels). Time between acute myocardial infarction to physiological interrogation was 5.9±2.4 days. Fractional flow reserve was similar in both groups (0.79±0.11 in non- IRA versus 0.80±0.13 in SA vessels, P=0.527). Lower coronary flow reserve values were found in non- IRA compared with SA vessels (1.77 [1.25-2.76] versus 2.44 [1.63-4.00], P=0.018), primarily driven by an increased baseline flow in non- IRA (rest mean transit time 0.58 [0.32-0.83] versus 0.65 s [0.39-1.20], P=0.045), whereas the hyperemic flow was similar (hyperemic mean transit time 0.26 [0.20-0.42] versus 0.26 s [0.18-0.35], P=0.873). No differences were found regarding index of microcirculatory resistance (15.6 [10.4-21.8] in non- IRA versus 16.7 [11.6-23.6] U in SA vessels, P=0.559). During adenosine infusion, the hyperemic response was similar in both groups (non- IRA versus SA vessels) in terms of the resistive reserve ratio (3.1±2.1 versus 3.7±2.2, P=0.118). Conclusions In the subacute phase of myocardial infarction, non- IRA show an increased baseline flow that may cause abnormal coronary flow reserve despite preserved hyperemic flow. In non- IRA , microcirculatory resistance and adenosine-induced hyperemic response are similar to those found in SA patients. From a physiological perspective, these findings support the use of fractional flow reserve to interrogate non- IRA during the subacute phase of myocardial infarction.

Keywords: coronary flow reserve; coronary microcirculation; fractional flow reserve; microcirculatory resistance; non‐infarct‐related arteries.

Figure 1

Study flowchart. AMI indicates acute myocardial infarction; non‐IRA, non‐infarct‐related arteries; SA, stable angina.

Figure 2

Distribution of diameter stenoses and FFR values in non‐IRA and SA. Box‐and‐whisker plots show similar stenoses severity as judged by percent diameter stenosis (%DS) (A) and FFR (B) between non‐IRA and the matched‐control SA target vessels. The boxes show the median and first and third quartiles. Red dashed lines indicate the corresponding mean values. FFR indicates fractional flow reserve; non‐IRA, non‐infarct‐related arteries; SA, stable angina.

Figure 3

Comparison of IMR values between non‐IRA and SA. A, Plot figure shows a similar distribution of IMR values in non‐IRA and the matched‐control SA target vessels. Dashed lines represent the mean value for IMR. B, The number of vessels with IMR ≥25 was similar in non‐IRA and SA. IMR indicates index of microcirculatory resistance; non‐IRA, non‐infarct‐related arteries; SA, stable angina.

Figure 4

Distribution of CFR values in non‐IRA and SA. A, CFR was significantly lower in non‐IRA as compared with that of the matched‐control group (SA target vessels). This difference can be explained when the components of CFR are analyzed separately: rest‐Tmn is significantly lower (higher flow) in non‐IRA (B), whereas hyperemic‐Tmn is very similar to that of SA target vessels (C). CFR indicates coronary flow reserve; Non‐IRA, non‐infarct‐related arteries; SA, stable angina; Tmn, mean transit time.

Figure 5

Correlation between FFR, IMR, and CFR according to the clinical presentation. A significant correlation (modest) was found between CFR and FFR in the SA group (A), but not in the non‐IRA (B). IMR was not correlated with FFR regardless of clinical presentation (C, D). CFR indicates coronary flow reserve; FFR, fractional flow reserve; IMR, index of microcirculatory resistance; non‐IRA, non‐infarct‐related arteries; SA, stable angina.

Figure 6

Hyperemic response to adenosine. A, In the non‐IRA, adenosine caused a drop of intracoronary distal pressure (delta Pd, from base to hyperemia) similar to that observed in the control matched group of SA‐vessels. Red dashed lines represent the estimated mean drop (delta) (Table 3). B, distribution of the RRR values in both groups. In this Box‐and‐whisker plots figure, the boxes show the median and first and third quartiles; * represents an outlier. Hyp indicates hyperemic; non‐IRA, non‐infarct‐related arteries; Pd, distal pressure; RRR, resistive reserve ratio; SA, stable angina.

Figure 7

Distribution of FFR, IMR, and CFR values in non‐IRA according to the type of acute myocardial infarction. In the non‐IRA, distribution of FFR, IMR, and CFR values was similar regardless of the type of acute myocardial infarction. Dashed lines represent mean values. CFR indicates coronary flow reserve; FFR, fractional flow reserve; IMR, index of microcirculatory resistance; NSTEMI, non–ST‐segment–elevation myocardial infarction; STEMI, ST‐segment–elevation myocardial infarction.