Microvascular resistance of the culprit coronary artery in acute ST-elevation myocardial infarction

Abstract

Background: Failed myocardial reperfusion is common and prognostically important after acute ST-elevation myocardial infarction (STEMI). The purpose of this study was to investigate coronary flow reserve (CFR), a measure of vasodilator capacity, and the index of microvascular resistance (IMR; mmHg × s) in the culprit artery of STEMI survivors.

Methods: IMR (n = 288) and CFR (n = 283; mean age [SD], 60 [12] years) were measured acutely using guide wire-based thermodilution. Cardiac MRI disclosed left ventricular pathology, function, and volumes at 2 days (n = 281) and 6 months after STEMI (n = 264). All-cause death or first heart failure hospitalization was independently adjudicated (median follow-up 845 days).

Results: Myocardial hemorrhage and microvascular obstruction occurred in 89 (42%) and 114 (54%) patients with evaluable T2*-MRI maps. IMR and CFR were associated with microvascular pathology (none vs. microvascular obstruction only vs. microvascular obstruction and myocardial hemorrhage) (median [interquartile range], IMR: 17 [12.0-33.0] vs. 17 [13.0-39.0] vs. 37 [21.0-63.0], P < 0.001; CFR: 1.7 [1.4-2.5] vs. 1.5 [1.1-1.8] vs. 1.4 [1.0-1.8], P < 0.001), whereas thrombolysis in myocardial infarction blush grade was not. IMR was a multivariable associate of changes in left ventricular end-diastolic volume (regression coefficient [95% CI] 0.13 [0.01, 0.24]; P = 0.036), whereas CFR was not (P = 0.160). IMR (5 units) was a multivariable associate of all-cause death or heart failure hospitalization (n = 30 events; hazard ratio [95% CI], 1.09 [1.04, 1.14]; P < 0.001), whereas CFR (P = 0.124) and thrombolysis in myocardial infarction blush grade (P = 0.613) were not. IMR had similar prognostic value for these outcomes as <50% ST-segment resolution on the ECG.

Conclusions: IMR is more closely associated with microvascular pathology, left ventricular remodeling, and health outcomes than the angiogram or CFR.

Trial registration: NCT02072850.

Funding: A British Heart Foundation Project Grant (PG/11/2/28474), the National Health Service, the Chief Scientist Office, a Scottish Funding Council Senior Fellowship, a British Heart Foundation Intermediate Fellowship (FS/12/62/29889), and a nonfinancial research agreement with Siemens Healthcare.

Figures

Figure 1. Three patients with acute ST-elevation myocardial infarction treated by primary percutaneous coronary intervention and with the same antithrombotic therapies, including aspirin, clopidogrel, heparin, and glycoprotein IIbIIIa inhibitor therapy with tirofiban.

Each patient had successful primary percutaneous coronary intervention (PCI), as evidenced by normal thrombolysis in myocardial infarction (TIMI) flow grade 3 the end of the procedure. Cardiac MRI was performed for each patient 2 days later. Coronary artery function was measured in 283 patients, of whom 281 (99%) had cardiac MRI and 213 (75%) had T2* MRI for assessment of myocardial hemorrhage. Top: A patient with normal index of microvascular resistance (IMR 2.0), and no evidence of microvascular injury on MRI. A diagnostic guide wire study of microvascular function in the territory of the culprit coronary artery immediately after primary PCI. IMR and CFR measurements were derived from coronary thermodilution. Microvascular function was normal (IMR 12, CFR 2.6), indicating successful myocardial reperfusion. Two days later, MRI ruled out myocardial hemorrhage (middle right image) or microvascular obstruction (right). Middle: A patient with normal IMR, low CFR, and microvascular obstruction but no hemorrhage on MRI 2 days later. The diagnostic guide wire study of culprit artery microvascular function at the end of primary PCI indicated an abnormal CFR (0.9) but a preserved IMR (11). Late gadolinium contrast-enhanced MRI revealed microvascular obstruction (right image, blue arrow). Bottom: A patient with high IMR, low CFR, and hemorrhagic infarction on MRI. The diagnostic guide wire study of culprit microvascular function immediately after primary PCI indicated severe microcirculatory dysfunction (IMR 89, CFR 1.0). T2*-MRI (middle right image) revealed myocardial hemorrhage (red arrow) within the infarct core. Contrast-enhanced MRI revealed microvascular obstruction (right image, red arrow) within the bright area of infarction. The microvascular obstruction within the infarct core spatially corresponded with the myocardial hemorrhage.

Figure 2. CONSORT flow diagram of the cohort study.

STEMI, ST-elevation myocardial infarction; CMR, cardiac magnetic resonance; CFR, coronary flow reserve; IMR, index of microvascular resistance.

Figure 3. An index of microvascular resistance and coronary flow reserve according to the presence or absence of myocardial hemorrhage and microvascular obstruction.

Top: An index of microvascular resistance (IMR) and coronary flow reserve (CFR) according to the presence (n = 89 [42%]) or absence (n = 124 [58%]) of myocardial hemorrhage in 213 participants who had T2* mapping with MRI 2 days after reperfusion. IMR was higher and CFR was lower in patients with myocardial hemorrhage (T2*MRI positive) compared to that in patients without myocardial hemorrhage (T2* MRI negative). Bottom: IMR and CFR according to the presence (n = 25) or absence of microvascular obstruction (n = 99) in the subset of patients from above without myocardial hemorrhage (n = 124 [58%]). In this subset of patients with less severe vascular injury, IMR was similar in patients with or without microvascular obstruction (MVO), as revealed by contrast-enhanced MRI. By contrast, CFR was lower in patients with MVO compared to CFR in patients without MVO. Mann-Whitney tests were used for the statistical analysis. In box-and-whisker plots, horizontal bars indicate the medians, boxes indicate 25th to 75th percentiles, and whiskers indicate 10th and 90th percentiles.