To assess the prognostic significance of infarct core tissue characteristics using cardiac magnetic resonance (CMR) imaging in survivors of acute ST-elevation myocardial infarction (STEMI).
Background— The use of fractional flow reserve (FFR) in acute coronary syndromes is controversial. The British Heart Foundation Fractional Flow Reserve Versus Angiography in Guiding Management to Optimize Outcomes in Non-ST-Elevation Myocardial Infarction (FAMOUS-NSTEMI) study (NCT01764334) has recently demonstrated the safety and feasibility of FFR measurement in patients with non–ST-segment–elevation myocardial infarction. We report the findings of the cardiac magnetic resonance (CMR) substudy to assess the diagnostic accuracy of FFR compared with 3.0-T stress CMR perfusion. Methods and Results— One hundred six patients with non–ST-segment–elevation myocardial infarction who had been referred for early invasive management were included from 2 centers. FFR was measured in all major patent epicardial coronary arteries with a visual stenosis estimated at ≥30%, and if percutaneous coronary intervention was performed, an FFR assessment was repeated. Myocardial perfusion was assessed with stress perfusion CMR at 3 T. The mean age was 56.7±9.8 years; 82.6% were men. Mean time from FFR evaluation to CMR was 6.1±3.1 days. The mean±SD left ventricular ejection fraction was 58.2±9.1%. Mean infarct size was 5.4±7.1%, and mean troponin concentration was 5.2±9.2 μg/L. There were 34 fixed and 160 inducible perfusion defects. There was a negative correlation between the number of segments with a perfusion abnormality and FFR ( r =−0.77; P <0.0001). The overall sensitivity, specificity, positive predictive value, and negative predictive value for an FFR of ≤0.8 were 91.4%, 92.2%, 76%, and 97%, respectively. Diagnostic accuracy was 92%. The positive and negative predictive values of FFR for flow-limiting coronary artery disease (FFR≤0.8) in patients with non–ST-segment–elevation myocardial infarction (n=21) who underwent perfusion CMR before invasive angiography were 92% and 93%, respectively. Receiver operating characteristic analysis indicated that the optimal cutoff value of FFR for demonstrating reversible ischemia on CMR was ≤0.805 (area under the receiver operating characteristic curve, 0.94 [0.9–0.99]; P <0.0001). Conclusions— FFR in patients with recent non–ST-segment–elevation myocardial infarction showed high concordance with myocardial perfusion in matched territories as revealed by 3.0-T stress perfusion CMR. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT02073422.
The jeopardised ischaemic area-at-risk (AAR) is a key prognostic determinant in acute myocardial infarction. Myocardial oedema imaging with T2-weighted cardiac magnetic resonance CMR is validated for imaging the AAR and T2 ‘mapping’ is a new method for AAR imaging with clinical and research potential. We aimed to develop an automated post-processing method that would enable straightforward volumetric quantification of AAR with T2 maps. Our approach retains user input (i.e. clinical judgement) to confirm the presence of oedema on an image which is then subjected to an automated analysis. The new method was tested on 12 acute MI patients who had a CMR within 48 hours of hospital admission. Manual segmentation of the left ventricular wall and oedema were available for comparison. Left ventricular wall boundaries were delineated automatically by variational level set methods followed by automated detection of myocardial oedema by fitting a Gaussian-Gaussian mixture statistical model. The mean perpendicular distances between automatically detected left ventricular boundaries and corresponding manual delineated boundaries were 1.8±0.2mm for endocardial boundaries and 2.3±0.3mm for endocardial boundaries. Dice similarity coefficients for agreement (0=no agreement, 1=perfect agreement) between manual delineation and automated segmentation of the left ventricular wall boundaries and oedema regions were 0.85±0.02 and 0.74±0.05, respectively. Compared to standard manual approaches, the new semi-automated method for estimating myocardial oedema is straightforward and accurate.
Background T1 and T2 cardiac magnetic resonance (CMR) mapping methods have shown promise for infarct characterisation in patients with acute ST-elevation myocardial infarction (STEMI). Non-ST elevation MI is typically a sub-acute problem with infarct characteristics that are less readily defined. We prospectively studied the diagnostic accuracy of two novel (T1, T2 mapping) and one established (T2 STIR) CMR methods for imaging the ischaemic area-at-risk (AAR) in patients with a recent NSTEMI. Methods NSTEMI patients underwent contrast-enhanced CMR at 3.0 Tesla (T) after percutaneous coronary intervention. The presence/extent of infarction was assessed with late gadolinium enhancement imaging (Gadovist, 0.1 mmol/kg). The infarct-related territory (IRA) was identified independently using a combination of angiographic, ECG and clinical findings. AAR was assessed with T1, T2 and T2 STIR methods by 2 observers who were blind to all of the clinical data. Comparisons were made between CMR and clinical findings. Results Seventy-three NSTEMI patients (mean age 57 ± 10 yrs, 78% male) underwent 3.0 T MRI. The mean infarct size was 5.5 ± 7.2% of left ventricular (LV) volume. The AAR T1 and T2 times were 1323 ± 68 ms and 57 ± 5 ms, respectively. The extent of AAR (% of LV volume) estimated with T1 (15.8 ± 10.6%) and T2 maps (16.0 ± 11.8%) was similar (p = 0.838), and moderately well correlated (r = 0.82, p Mean AAR estimated with T2 STIR (7.8 ± 11.6%) was lower than that estimated with T1 (p The IRA was correctly identified in 52 patients (71%) when with T1 CMR, 56 (77%) with T2 CMR, and 32 (44%) with T2 STIR CMR. The diagnostic accuracies of T1 and T2 CMR for identification of the IRA were similar (p = 0.125) whereas T1 CMR and T2 CMR had higher diagnostic accuracy vs. T2 STIR (both p Conclusion T1 and T2 maps have higher diagnostic accuracy than T2 STIR maps, implying superior clinical utility with T1 and T2 CMR for infarct characterisation in NSTEMI patients.
Cardiac magnetic resonance (CMR) imaging enables the assessment of left ventricular function and pathology. In addition to established contrast-enhanced methods for the assessment of infarct size and microvascular obstruction, other infarct pathologies, such as myocardial edema and myocardial hemorrhage, can be identified using innovative CMR techniques. The initial extent of myocardial edema revealed by T2-weighted CMR has to be stable for edema to be taken as a retrospective marker of the area-at-risk, which is used to calculate myocardial salvage. The timing of edema assessment is important and should be focused within 2 - 7 days post-reperfusion. Some recent investigations have called into question the diagnostic validity of edema imaging after acute STEMI. Considering the results of these studies, as well as results from our own laboratory, we conclude that the time-course of edema post-STEMI is unimodal, not bimodal. Myocardial hemorrhage is the final consequence of severe vascular injury and a progressive and prognostically important complication early post-MI. Myocardial hemorrhage is a therapeutic target to limit reperfusion injury and infarct size post-STEMI.
The effects of ethanol on brain function have been extensively studied using a variety of in vitro and in vivo techniques. For example, electrophysiological studies using brain slices from rodents and nonhuman primates have demonstrated that acute and chronic exposure to ethanol alters the intrinsic excitability and synaptic signaling of neurons within cortical and sub-cortical areas of the brain. In humans, neuroimaging studies reveal alterations in measures of brain activation and connectivity in subjects with alcohol use disorders. While complementary, these methods are inherently limited due to issues related to either disruption of normal sensory input (in vitro slice studies) or resolution (whole brain imaging). In the present study, we used 2-photon laser scanning microscopy in intact animals to assess the impact of chronic ethanol exposure on sensory evoked neuronal and vascular responses. Adult male C57BL/6J mice were exposed to 4 weekly cycles of chronic intermittent ethanol (CIE) exposure while control mice were exposed to air. After withdrawal (≥ 72 hr), a cranial window was placed over the primary visual cortex (V1) and sensory evoked responses were monitored using the calcium indicator OGB-1. CIE exposure produced small but significant changes in response amplitude (decrease) and orientation selectivity of V1 neurons (increase). While arteriole diameter did not differ between control and CIE mice under baseline conditions, vessels in CIE exposed mice showed enhanced sensory-evoked dilation as compared to controls. This was accompanied by a reduced latency in response to stimulation. In separate experiments, pial arteriole diameter was measured in the barrel cortex of control and CIE exposed mice. Baseline diameter of barrel cortex arterioles was similar between control and CIE exposed mice but unlike vessels in V1, no changes were noted in barrel cortex arteriole diameter following sensory stimulation. Together the results of these studies suggest that chronic exposure to alcohol induces changes in neurovascular coupling that are region dependent.
Displacement encoding with stimulated echoes (DENSE) encodes myocardial tissue displacement into the phase of the MRI image permitting direct quantification of myocardial displacement at multiple cardiac phases. Strain-encoded CMR with DENSE has high spatial (3.2 mm × 3.2 mm × 8 mm) and temporal resolution (TR= 27.34 ms). We aimed to measure myocardial strain values with DENSE in healthy adults across a broad age range at 3.0Tesla.
Methods
Healthy volunteers with no prior medical history or treatment were enrolled and underwent CMR at 3.0T (Magnetom Verio, Siemens, Erlangen, Germany). Mid-left ventricular short axis and horizontal long axis DENSE sequences were obtained, and analysed using CIM_DENSE2D software (University of Auckland, New Zealand and Siemens Healthcare). Segmental and global myocardial circumferential (Ecc) and longitudinal (Ell) strain were obtained with DENSE.
Results
77 participants (mean (SD) age 43.0(16.9) years; range 18–78 years; 40 (52%) males;) were grouped into 3 tertiles according to age. Longitudinal strain differed according to age tertile with strain being greatest in individuals 35–55 years compared to younger or older subjects. There were no differences in Ecc according to age per tertile (Table 1).
Conclusion
Longitudinal myocardial strain, as revealed by strain-encoded CMR, is associated with chronological age in healthy adults.
Funding
Medical Research Scotland project grant. Professor Berry was supported by a Senior Clinical Fellowship from the Scottish Funding Council.
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