Purpose To develop a deep learning model for increasing cardiac cine frame rate while maintaining spatial resolution and scan time. Materials and Methods A transformer-based model was trained and tested on a retrospective sample of cine images from 5840 patients (mean age, 55 years ± 19 [SD]; 3527 male patients) referred for clinical cardiac MRI from 2003 to 2021 at nine centers; images were acquired using 1.5- and 3-T scanners from three vendors. Data from three centers were used for training and testing (4:1 ratio). The remaining data were used for external testing. Cines with downsampled frame rates were restored using linear, bicubic, and model-based interpolation. The root mean square error between interpolated and original cine images was modeled using ordinary least squares regression. In a prospective study of 49 participants referred for clinical cardiac MRI (mean age, 56 years ± 13; 25 male participants) and 12 healthy participants (mean age, 51 years ± 16; eight male participants), the model was applied to cines acquired at 25 frames per second (fps), thereby doubling the frame rate, and these interpolated cines were compared with actual 50-fps cines. The preference of two readers based on perceived temporal smoothness and image quality was evaluated using a noninferiority margin of 10%. Results The model generated artifact-free interpolated images. Ordinary least squares regression analysis accounting for vendor and field strength showed lower error (
Non-ischaemic cardiomyopathies (NICMs) are chronic, progressive myocardial diseases with distinct patterns of morphological, functional, and electrophysiological changes. In the setting of cardiomyopathy (CM), determining the exact aetiology is important because the aetiology is directly related to treatment and patient survival. Determining the exact aetiology, however, can be difficult using currently available imaging techniques, such as echocardiography, radionuclide imaging or X-ray coronary angiography, since overlap of features between CMs may be encountered. Cardiovascular magnetic resonance (CMR) imaging has recently emerged as a new non-invasive imaging modality capable of providing high-resolution images of the heart in any desired plane. Delayed contrast enhanced CMR (DE-CMR) can be used for non-invasive tissue characterization and may hold promise in differentiating ischaemic from NICMs, as the typical pattern of hyperenhancement can be classified as ‘ischaemic-type’ or ‘non-ischaemic type’ on the basis of pathophysiology of ischaemia. This article reviews the potential of DE-CMR to distinguish between ischaemic and NICM as well as to differentiate non-ischaemic aetiologies. Rather than simply describing various hyperenhancement patterns that may occur in different disease states, our goal will be (i) to provide an overall imaging approach for the diagnosis of CM and (ii) to demonstrate how this approach is based on the underlying relationships between contrast enhancement and myocardial pathophysiology.
Although magnetic resonance first-pass imaging (MRFP) has potential advantages in pharmacological stress perfusion imaging, direct comparisons of current MRFP and established radionuclide techniques are not available.Graded regional differences in coronary flow were produced during global coronary vasodilation in chronically instrumented dogs by partially occluding the left circumflex artery. Regional differences in full-thickness flow quantified using microspheres were compared with regional differences obtained with MRFP and radionuclide SPECT imaging (99mTc-sestamibi and 201Tl). Relative regional flows (RRFs) derived from the initial areas under MRFP signal intensity-time curves were linearly related to reference microsphere RRFs over the full range of vasodilation (y=0.93x+4.3; r2=0.77). Relationships between 99mTc-sestamibi and 201Tl RRFs and microsphere RRFs were curvilinear, plateauing as flows increased. The high spatial resolution of the MRI enabled transmural flow to be evaluated in 3 to 5 layers across the myocardial wall. Reductions in subendocardial flow were visually apparent in MRFP images for > or =50% reductions in full-thickness flow. Endocardial-to-epicardial gradients in MRFP flow increased progressively with stenosis severity, whereas transmural flow patterns in remote normally perfused myocardium remained normal. Flow reductions of > or =50% not identified by radionuclide imaging were apparent in MRFP full-thickness and transmural analyses.High-resolution MRFP can identify regional reductions in full-thickness myocardial blood flow during global coronary vasodilation over a wider range than current SPECT imaging. Transmural flow gradients can also be identified; their magnitude increases progressively as flow limitations become more severe and endocardial flow is compromised increasingly.
To compare the utility and efficacy of stress cardiac magnetic resonance (MR) imaging and stress echocardiography in an emergency setting in patients with acute chest pain (CP) and intermediate risk of coronary artery disease (CAD).Written informed consent was obtained from all patients. This HIPAA-compliant study was approved by the institutional review board for research ethics. Sixty patients without history of CAD presented to the emergency department with intermediate-risk acute CP and were prospectively enrolled. Patients underwent both stress cardiac MR imaging and stress echocardiography in random order within 12 hours of presentation. Stress imaging results were interpreted clinically immediately (blinded interpretation was performed months later), and coronary angiography was performed if either result was abnormal. CAD was considered significant if it was identified at angiography (narrowing >50% ) or if a cardiac event (death or myocardial infarction) occurred during follow-up (mean, 14 months ± 5 [standard deviation]). McNemar test was used to compare the diagnostic accuracy of techniques.Stress cardiac MR imaging and stress echocardiography had similar specificity, accuracy, and positive and negative predictive values (92% vs 96%, 93% vs 88%, 67% vs 60%, and 100% vs 91%, respectively, for clinical interpretation; 90% vs 92%, 90% vs 88%, 58% vs 56%, and 98% vs 94%, respectively, for blinded interpretation). Stress cardiac MR imaging had higher sensitivity at clinical interpretation (100% vs 38%, P = .025), which did not reach significance at blinded interpretation (88% vs 63%, P = .31). However, multivariable logistic regression analysis showed stress cardiac MR imaging to be the strongest independent predictor of significant CAD (P = .002).In patients presenting to the emergency department with intermediate-risk CP, adenosine stress cardiac MR imaging performed within 12 hours of presentation is safe and potentially has improved performance characteristics compared with stress echocardiography. Online supplemental material is available for this article.
Objective: The effect of coronary perfusion on left ventricular chamber distensibility is only indirect evidence that perfusion alters the mechanical properties of the myocardium. The aim of this study was to demonstrate explicitly the effects of coronary perfusion on these mechanical properties. Methods: The effects of different levels of coronary perfusion were studied both on in-plane stress-strain relations and on transverse stiffness in an isolated, perfused canine interventricular septal preparation. Additionally, to determine the vascular compartment responsible for the mechanical effects of perfusion on tissue properties, we examined the in-plane stress-strain responses and transverse stiffness after embolisation of the vasculature with 15 μm microspheres. Results: The data show a clear dependence of tissue stress-strain properties on perfusion. The in-plane stress-strain relations were shifted to the left and transverse stiffness increased linearly as septal artery perfusion pressure increased. The dependence of both the in-plane stress-strain relations and transverse stiffness on perfusion was significantly decreased following embolisation. Conclusions: Myocardial tissue stiffness is directly related to perfusion. The linear relationship between transverse stiffness and perfusion makes it easier to assess the effects of perfusion on tissue stiffness than with in-plane stress-strain relations. Perfusion of capillaries and/or venules is largely responsible for these alterations in myocardial stiffness. Cardiovascular Research 1993;27:403-410
tional but viable myocardium may improve left ventricular function and long-term survival [1][2][3] .Non-contractile yet viable myocardium can be caused by acute, subacute and chronic states of abnormalities of myocardial perfusion.Frequently used paradigms to describe dysfunctional viable myocardium are stunning and hibernation, which both refer to reversible left ventricular contraction impairment.Hibernation describes the concomitant reduction of perfusion and contractility, whereas stunning characterizes contractile impairment persisting after complete return of blood flow.Stunning has been observed in many clinical situations, such as unstable angina [4] , exercised-induced ischaemia [5] , after cardioplegic solution has been used during cardiac surgery [6] , and in the early period after successful reperfusion of an acute myocardial infarction patient [7] .Hibernation is thought to be characterized by chronically reduced coronary perfusion.It is believed to represent an adapted state in which contractile function is diminished in order to match the decreased supply of substrates and oxygen to the myocardium.There are several reasons why it is important to distinguish between viable and infarcted myocardium.First, patient prognosis is altered.Several studies have shown that patients with acute ventricular dysfunction, primarily due to myocardial necrosis, have a worse prognosis than patients with reversible ventricular dysfunction [8,9] .Second, patient management during the acute setting could be changed.Viable but injured myocardium, such as stunned myocardium, is potentially at risk for future infarction if there is significant residual stenosis following reperfusion therapy [8,10] .Additionally, determination of the extent of viable as compared to non-viable myocardium across the ventricular wall in a dysfunctional region may be valuable in selecting patients most likely to benefit from therapy, such as angiotensin-converting enzyme inhibitors [11] that can modulate ventricular remodelling after acute infarction.Third, infarct size determined accurately in the acute setting may prove to be an adequate surrogate end-point for the assessment of new therapies [12,13] .This suggests, for example, that the efficacy of current and experimental reperfusion therapies could be evaluated without requiring 'mega' trials with large sample sizes that use mortality as an end-point.This review will outline how cardiovascular magnetic resonance distinguishes between viable and necrotic myocardium and will describe how magnetic resonance imaging provides new approaches to the diagnosis and the treatment of patients with ischaemic left ventricular dysfunction. Definition of myocardial viabilityThe clinical question of viability will arise in a patient with severely dysfunctional myocardium and ischaemic heart disease.In such patients the definition of myocardial viability is directly related to that of myocardial infarction because infarction is defined as the loss of viability.In the clinical setting, a number of techniques
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