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      Invasive Assessment of the Coronary Microcirculation in Reperfused ST-Segment–Elevation Myocardial Infarction Patients : Where Do We Stand?

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          Abstract

          For patients presenting with an acute ST-segment-elevation myocardial infarction, the most effective therapy for reducing myocardial infarct size and preserving left ventricular systolic function is primary percutaneous coronary intervention (PPCI). However, mortality and morbidity remain significant. This is partly attributed to the development of microvascular obstruction, which occurs in around 50% of ST-segment-elevation myocardial infarction patients post-PPCI, and it is associated with adverse left ventricular remodeling and worse clinical outcomes. Although microvascular obstruction can be detected by cardiac imaging techniques several hours post-PPCI, it may be too late to intervene at that time. Therefore, being able to predict the development of microvascular obstruction at the time of PPCI may identify high-risk patients who might benefit from further adjuvant intracoronary therapies, such as thrombolysis, vasodilators, glycoprotein IIb/IIIa inhibitors, and anti-inflammatory agents that may reduce microvascular obstruction. Recent studies have shown that invasive coronary physiology measurements performed during PPCI can be used to assess the coronary microcirculation. In this article, we provide an overview of the various invasive methods currently available to assess the coronary microcirculation in the setting of ST-segment-elevation myocardial infarction, and how they could potentially be used in the future for tailoring therapies to those most at risk.

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          Most cited references 64

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          Novel index for invasively assessing the coronary microcirculation.

          A relatively simple, invasive method for quantitatively assessing the status of the coronary microcirculation independent of the epicardial artery is lacking. By using a coronary pressure wire and modified software, it is possible to calculate the mean transit time of room-temperature saline injected down a coronary artery. The inverse of the hyperemic mean transit time has been shown to correlate with absolute flow. We hypothesize that distal coronary pressure divided by the inverse of the hyperemic mean transit time provides an index of microcirculatory resistance (IMR) that will correlate with true microcirculatory resistance (TMR), defined as the distal left anterior descending (LAD) pressure divided by hyperemic flow, measured with an external ultrasonic flow probe. A total of 61 measurements were made in 9 Yorkshire swine at baseline and after disruption of the coronary microcirculation, both with and without an epicardial LAD stenosis. The mean IMR (16.9+/-6.5 U to 25.9+/-14.4 U, P=0.002) and TMR (0.51+/-0.14 to 0.79+/-0.32 mm Hg x mL(-1) x min(-1), P=0.0001), as well as the % change in IMR (147+/-66%) and TMR (159+/-105%, P=NS versus IMR % change), increased significantly and to a similar degree after disruption of the microcirculation. These changes were independent of the status of the epicardial artery. There was a significant correlation between mean IMR and TMR values, as well as between the % change in IMR and % change in TMR. Measuring IMR may provide a simple, quantitative, invasive assessment of the coronary microcirculation.
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            Is Open Access

            Myocardial Hemorrhage After Acute Reperfused ST-Segment–Elevation Myocardial Infarction

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              Prognostic value of the Index of Microcirculatory Resistance measured after primary percutaneous coronary intervention.

              Most methods for assessing microvascular function are not readily available in the cardiac catheterization laboratory. The aim of this study is to determine whether the Index of Microcirculatory Resistance (IMR), measured at the time of primary percutaneous coronary intervention, is predictive of death and rehospitalization for heart failure. IMR was measured immediately after primary percutaneous coronary intervention in 253 patients from 3 institutions with the use of a pressure-temperature sensor wire. The primary end point was the rate of death or rehospitalization for heart failure. The prognostic value of IMR was compared with coronary flow reserve, TIMI myocardial perfusion grade, and clinical variables. The mean IMR was 40.3±32.5. Patients with an IMR >40 had a higher rate of the primary end point at 1 year than patients with an IMR ≤40 (17.1% versus 6.6%; P=0.027). During a median follow-up period of 2.8 years, 13.8% experienced the primary end point and 4.3% died. An IMR >40 was associated with an increased risk of death or rehospitalization for heart failure (hazard ratio [HR], 2.1; P=0.034) and of death alone (HR, 3.95; P=0.028). On multivariable analysis, independent predictors of death or rehospitalization for heart failure included IMR >40 (HR, 2.2; P=0.026), fractional flow reserve ≤0.8 (HR, 3.24; P=0.008), and diabetes mellitus (HR, 4.4; P 40 was the only independent predictor of death alone (HR, 4.3; P=0.02). An elevated IMR at the time of primary percutaneous coronary intervention predicts poor long-term outcomes.
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                Author and article information

                Journal
                Circulation: Cardiovascular Interventions
                Circ Cardiovasc Interv
                Ovid Technologies (Wolters Kluwer Health)
                1941-7640
                1941-7632
                March 2017
                March 2017
                : 10
                : 3
                Affiliations
                [1 ]From the Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, United Kingdom (H.B., D.J.H.); The National Institute of Health Research, University College London Hospitals, Biomedical Research Centre, United Kingdom (H.B., D.J.H.); Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore (H.B., N.F., D.J.H.); National Heart Research Institute Singapore, National Heart Centre Singapore (H.B., N.F., J.W.T., D.J.H.); National...
                Article
                10.1161/CIRCINTERVENTIONS.116.004373
                28242607
                © 2017

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