Microvascular Resistance Predicts Myocardial Salvage and Infarct Characteristics in ST‐Elevation Myocardial Infarction

Payne, A. P.; Berry, Colin; Doolin, Orla; McEntegart, Margaret; Petrie, Mark C; Lindsay, Mitchell; Hood, Stuart; Carrick, David; Tzemos, Niko; Weale, Peter; McComb, Christie; Foster, John E.; Ford, Ian; Oldroyd, Keith G.

doi:10.1161/jaha.112.002246

Cited by 85 publications

(82 citation statements)

References 34 publications

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“…Myocardial salvage was calculated by subtraction of percentage of infarct size from percentage of area at risk 13, 40. The myocardial salvage index was calculated by dividing the myocardial salvage area by the initial area at risk.…”

Section: Methodsmentioning

confidence: 99%

Temporal Evolution of Myocardial Hemorrhage and Edema in Patients After Acute ST‐Segment Elevation Myocardial Infarction: Pathophysiological Insights and Clinical Implications

Carrick

Haig

Ahmed

et al. 2016

JAHA

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108

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BackgroundThe time course and relationships of myocardial hemorrhage and edema in patients after acute ST‐segment elevation myocardial infarction (STEMI) are uncertain.Methods and ResultsPatients with ST‐segment elevation myocardial infarction treated by primary percutaneous coronary intervention underwent cardiac magnetic resonance imaging on 4 occasions: at 4 to 12 hours, 3 days, 10 days, and 7 months after reperfusion. Myocardial edema (native T2) and hemorrhage (T2*) were measured in regions of interest in remote and injured myocardium. Myocardial hemorrhage was taken to represent a hypointense infarct core with a T2* value <20 ms. Thirty patients with ST‐segment elevation myocardial infarction (mean age 54 years; 25 [83%] male) gave informed consent. Myocardial hemorrhage occurred in 7 (23%), 13 (43%), 11 (33%), and 4 (13%) patients at 4 to 12 hours, 3 days, 10 days, and 7 months, respectively, consistent with a unimodal pattern. The corresponding median amounts of myocardial hemorrhage (percentage of left ventricular mass) during the first 10 days after myocardial infarction were 2.7% (interquartile range [IQR] 0.0–5.6%), 7.0% (IQR 4.9–7.5%), and 4.1% (IQR 2.6–5.5%; P<0.001). Similar unimodal temporal patterns were observed for myocardial edema (percentage of left ventricular mass) in all patients (P=0.001) and for infarct zone edema (T2, in ms: 62.1 [SD 2.9], 64.4 [SD 4.9], 65.9 [SD 5.3]; P<0.001) in patients without myocardial hemorrhage. Alternatively, in patients with myocardial hemorrhage, infarct zone edema was reduced at day 3 (T2, in ms: 51.8 [SD 4.6]; P<0.001), depicting a bimodal pattern. Left ventricular end‐diastolic volume increased from baseline to 7 months in patients with myocardial hemorrhage (P=0.001) but not in patients without hemorrhage (P=0.377).ConclusionsThe temporal evolutions of myocardial hemorrhage and edema are unimodal, whereas infarct zone edema (T2 value) has a bimodal pattern. Myocardial hemorrhage is prognostically important and represents a target for therapeutic interventions that are designed to preserve vascular integrity following coronary reperfusion.Clinical Trial Registration URL: https://clinicaltrials.gov/. Unique identifier: NCT02072850.

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Section: Methodsmentioning

confidence: 99%

Temporal Evolution of Myocardial Hemorrhage and Edema in Patients After Acute ST‐Segment Elevation Myocardial Infarction: Pathophysiological Insights and Clinical Implications

Carrick

Haig

Ahmed

et al. 2016

JAHA

Self Cite

108

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“…Of note, in that study not only patients with primary PCI but also patients with successful thrombolysis or rescue PCI after failed thrombolysis were included. Payne et al 36 showed that IMR was linked to MVI as assessed by CMR in a more homogeneous group of patients with STEMI treated by primary PCI. Doppler-flow velocity is an alternative technique to measure microvascular resistance.…”

Section: Measurements Of Coronary Flow and Microvascular Resistance Imentioning

confidence: 99%

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

Teunissen

Waard

Hollander

et al. 2015

Circ: Cardiovascular Interventions

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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...

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“…Myocardial salvage was calculated by subtraction of percentage infarct size from percentage area at risk, as reflected by the extent of edema 23, 26, 27. The myocardial salvage index was calculated by dividing the myocardial salvage area by the initial area at risk.…”

Section: Methodsmentioning

confidence: 99%

Coronary Thermodilution Waveforms After Acute Reperfused ST‐Segment–Elevation Myocardial Infarction: Relation to Microvascular Obstruction and Prognosis

Yew

Carrick

Corcoran

et al. 2018

JAHA

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BackgroundInvasive measures of microvascular resistance in the culprit coronary artery have potential for risk stratification in acute ST‐segment–elevation myocardial infarction. We aimed to investigate the pathological and prognostic significance of coronary thermodilution waveforms using a diagnostic guidewire.Methods and ResultsCoronary thermodilution was measured at the end of percutaneous coronary intervention, (PCI) and contrast‐enhanced cardiac magnetic resonance imaging (MRI) was intended on day 2 and 6 months later to assess left ventricular (LV) function and pathology. All‐cause death or first heart failure hospitalization was a pre‐specified outcome (median follow‐up duration 1469 days). Thermodilution recordings underwent core laboratory assessment. A total of 278 patients with acute ST‐segment elevation myocardial infarction EMI (72% male, 59±11 years) had coronary thermodilution measurements classified as narrow unimodal (n=143 [51%]), wide unimodal (n=100 [36%]), or bimodal (n=35 [13%]). Microvascular obstruction and myocardial hemorrhage were associated with the thermodilution waveform pattern (P=0.007 and 0.011, respectively), and both pathologies were more prevalent in patients with a bimodal morphology. On multivariate analysis with baseline characteristics, thermodilution waveform status was a multivariable associate of microvascular obstruction (odds ratio [95% confidence interval]=5.29 [1.73, 16.22];, P=0.004) and myocardial hemorrhage (3.45 [1.16, 10.26]; P=0.026), but the relationship was not significant when index of microvascular resistance (IMR) >40 or change in index of microvascular resistance (5 per unit) was included. However, a bimodal thermodilution waveform was independently associated with all‐cause death and hospitalization for heart failure (odds ratio [95% confidence interval]=2.70 [1.10, 6.63]; P=0.031), independent of index of microvascular resistance>40, ST‐segment resolution, and TIMI (Thrombolysis in Myocardial Infarction) Myocardial Perfusion Grade.ConclusionsThe thermodilution waveform in the culprit coronary artery is a biomarker of prognosis and may be useful for risk stratification immediately after reperfusion therapy.

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Microvascular Resistance Predicts Myocardial Salvage and Infarct Characteristics in ST‐Elevation Myocardial Infarction

Abstract: Background--The pathophysiology of myocardial injury and repair in patients with ST-elevation myocardial infarction is incompletely understood. We investigated the relationships among culprit artery microvascular resistance, myocardial salvage, and ventricular function.

Cited by 85 publications

References 34 publications

Temporal Evolution of Myocardial Hemorrhage and Edema in Patients After Acute ST‐Segment Elevation Myocardial Infarction: Pathophysiological Insights and Clinical Implications

Temporal Evolution of Myocardial Hemorrhage and Edema in Patients After Acute ST‐Segment Elevation Myocardial Infarction: Pathophysiological Insights and Clinical Implications

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

Coronary Thermodilution Waveforms After Acute Reperfused ST‐Segment–Elevation Myocardial Infarction: Relation to Microvascular Obstruction and Prognosis

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