Doppler-Derived Intracoronary Physiology Indices Predict the Occurrence of Microvascular Injury and Microvascular Perfusion Deficits After Angiographically Successful Primary Percutaneous Coronary Intervention

Abstract

Background-A total of40% to 50% of patients with ST-segment-elevation myocardial infarction develop microvascular injury (MVI) despite angiographically successful primary percutaneous coronary intervention (PCI). We investigated whether hyperemic microvascular resistance (HMR) immediately after angiographically successful PCI predicts MVI at cardiovascular magnetic resonance and reduced myocardial blood flow at positron emission tomography (PET). Methods and Results-Sixty patients with ST-segment-elevation myocardial infarction were included in this prospective study. Immediately after successful PCI, intracoronary pressure-flow measurements were performed and analyzed off-line to calculate HMR and indices derived from the pressure-velocity loops, including pressure at zero flow. Cardiovascular magnetic resonance and H 2 15O PET imaging were performed 4 to 6 days after PCI. Using cardiovascular magnetic resonance, MVI was defined as a subendocardial recess of myocardium with low signal intensity within a gadoliniumenhanced area. Myocardial perfusion was quantified using H 2 15 O PET. Reference HMR values were obtained in 16 stable patients undergoing coronary angiography. Complete data sets were available in 48 patients of which 24 developed MVI. Adequate pressure-velocity loops were obtained in 29 patients. HMR in the culprit artery in patients with MVI was significantly higher than in patients without MVI (MVI, 3.33±1.50 mm Hg/cm per second versus no MVI, 2.41±1.26 mm Hg/cm per second; P=0.03). MVI was associated with higher pressure at zero flow (45.68±13.16 versus 32.01±14.98 mm Hg; P=0.015). Multivariable analysis showed HMR to independently predict MVI (P=0.04). The optimal cutoff value for HMR was 2.5 mm Hg/cm per second. High HMR was associated with decreased myocardial blood flow on PET (myocardial perfusion reserve <2.0, 3.18±1.42 mm Hg/cm per second versus myocardial perfusion reserve ≥2.0, 2.24±1.19 mm Hg/cm per second; P=0.04). 1 CMRdefined MVI is assessed by T2-weighted imaging and late gadolinium enhancement. MVI refers to the areas within the infarcted myocardium where wash-in of contrast medium is severely impaired, as opposed to the wash-in (and delayed wash-out) of the contrast medium in the remaining areas of the infarct. It has been postulated that within these areas devoid of contrast, the microvasculature is obstructed, hence the term microvascular obstruction. Recently, however, it was shown that CMR-defined microvascular obstruction actually contains intramyocardial hemorrhage and complete microvascular destruction. Conclusions-Doppler2 Therefore, the term MVI seems to be more appropriate.The occurrence of MVI is linked to negative remodeling and left ventricular dysfunction, leading to decreased longterm survival, increased morbidity, and reduced quality of life as compared with patients with ST-segment-elevation myocardial infarction (STEMI) without MVI.3 MVI is related to ischemia-reperfusion damage and can potentially be reversed by pharmacological treatment in addition to the stand...

In vivo assessment of myocardial viability after acute myocardial infarction: A head-to-head comparison of the perfusable tissue index by PET and delayed contrast-enhanced CMR

“…STEMI was defined according to the European Society of Cardiology/ACCF/AHA/World Heart Federation Task Force for the Universal Definition of Myocardial Infarction as new ST elevation at the J point in at least 2 contiguous leads of ≥2 mm (0.2 mV) in men or ≥1.5 mm (0.15 mV) in women in leads V2-V3 and/or of ≥1 mm (0.1 mV) in other contiguous chest leads or the limb leads, in the absence of left ventricular (LV) hypertrophy or left bundle-branch block (LBBB) 9. As described previously,10 all patients were treated according to the ESC guidelines for management of STEMI 11. Patients with three-vessel disease and those who were hemodynamically unstable were excluded, since repeat revascularization therapies were deemed probable during study follow-up.…”

Hyperaemic microvascular resistance predicts clinical outcome and microvascular injury after myocardial infarction

“…The fact that HMR is immediately available after revascularisation is of paramount importance, since a window for adjunctive therapy still exists. Physiological measurements in non-culprit vessels also provide prognostic information,26 but are not indicative of CMR-defined MVI 10…”

Heart failure after myocardial infarction in the era of primary percutaneous coronary intervention: Mechanisms, incidence and identification of patients at risk

“…IMR is now being used as a surrogate endpoint in ongoing trials of aspiration thrombectomy and intracoronary GpIIb/IIIa agents[55]. Hyperaemic microvascular resistance (HMR), another specific read-out of microcirculatory function, is also predictive of CMR-defined microvascular occlusion (MVO), and impaired local blood flow as measured by PET[56]. …”

“…Pzf, derived from pressure-velocity loop analysis, is the distal coronary pressure at which the flow in a coronary artery would theoretically cease and represents extravascular compression of the microcirculation by oedema or haemorrhage. Pzf correlates with HMR, and also predicts residual scar at 6 mo post-MI with an AUC of 0.94[56,58]. FFR, the ratio of myocardial blood flow at maximal hyperaemia in comparison to normal proximal myocardial flow, is also predictive of adverse outcome, with an FFR of ≤ 0.8 associated with an HR of 3.24 for MACE[58].…”