Lipomatous metaplasia in myocardial infarction detected by cardiovascular magnetic resonance.
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Biomedical subjects
Publications and source records attributed to A C van Rossum.
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Earlier studies have shown substantial nonuniformity in normal left ventricular (LV) myocardial function concerning both the degree of shortening and timing of shortening. We hypothesized that nonuniform LV function may be related to nonuniform prestretch induced by atrial contraction. Eleven healthy human subjects were studied using MRI myocardial tagging and strain analysis. The amount of circumferential prestretch was assessed in 30 LV segments. Prestretch was defined as the difference in strain between end diastole (at ECG R wave) and diastasis. Furthermore, both the degree of shortening (quantified as peak circumferential shortening, peak systolic shortening rate, and amount of postsystolic shortening) and timing of shortening (quantified as the onset time of shortening and time to peak shortening) were assessed. LV prestretch was found to be nonuniform, with the highest values in the lateral wall. The amount of segmental prestretch correlated significantly with peak shortening (r = 0.79), peak shortening rate (r = 0.50), amount of postsystolic shortening (r = 0.67), onset time of shortening (r = -0.57), and time to peak shortening (r = 0.71) (P < 0.001 for each of these relations). These relations may be explained by regional differences in wall stress or by a regional Frank-Starling effect. The correlation between timing of shortening and prestretch demonstrates that mechanical timing is not determined by electrical phenomena alone. In conclusion, regional variation in LV function correlates with the nonuniform prestretch from atrial contraction.
Mechanical asynchrony is an important parameter in predicting the response to cardiac resynchronization therapy, but detailed knowledge of cardiac contraction timing in healthy persons is scarce. In this work, timing of cardiac contraction was mapped in 17 healthy subjects with high-temporal-resolution (14 ms) MRI myocardial tagging and strain analysis. Both the onset time of circumferential shortening (T(onset)) in early systole and the time of peak circumferential shortening (T(peak)) at end systole were determined. The onset of shortening width (time needed for 20-90% of the left ventricle to start shortening) was small (35 +/- 9 ms). A distinct spatial pattern for T(onset) was found, with earliest onset in the lateral wall and latest onset in the septum (P = 0.001). Compared with T(onset), T(peak) had a larger width (121 +/- 22 ms) and an opposite spatial pattern, with peak shortening occurring earlier in the septum than in the lateral wall (P < 0.001). Postsystolic shortening (T(peak) later than aortic valve closure; P < 0.05) was observed in 13 of the 30 cardiac segments, mainly in the lateral and basal segments. Shortening in these segments continued 58 +/- 14 ms after aortic valve closure, during which circumferential shortening increased from 16.9 +/- 1.2% to 20.0 +/- 1.5%. Maps of the timing of contraction in normal subjects may serve as a reference in detecting mechanical asynchrony due to intraventricular conduction defects or ischemia.
Hypertrophic cardiomyopathy (HCM) is a cardiac muscle disease with characteristic (mostly asymmetrically distributed) hypertrophy of a non-dilated left ventricle in the absence of another cardiac or systemic disease that can cause left ventricle hypertrophy. The prevalence of HCM in the general population is estimated to be 1 in 500 persons. It is an inheritable disease of the heart with a heterogeneous expression and a great diversity of morphological, functional and clinical features. The genes involved code for components of a large protein complex ('the sarcomere'), which ensures the contraction of the cardiac muscle. Electrocardiography, echocardiography and cardiac MRI play a role in the diagnosis. Medicinal treatment can improve the diastolic filling and the ventricle function. In addition to this there are surgical and non-surgical possibilities for myocardial reduction. For patients with life-threatening arrhythmias and for the primary prevention of sudden death for high-risk patients, an internally implantable cardioverter-defibrillator is indicated. The early detection of patients with a predisposition for HCM is only possible by means of genotyping.
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OBJECTIVES: Using two-dimensional wall thickening (WT) (expressed as percentage) and strain analysis, regional contractile myocardial function was quantified and compared in 13 control subjects and 13 patients with a first myocardial infarction (MI). The findings in the patient group were related to global ventricular function and infarct size. BACKGROUND: In patients with coronary artery disease, regions with dysfunctional myocardium cannot be differentiated easily from regions with normal function by planar WT analysis. Physiologic factors, in combination with limitations of conventional imaging techniques, affect the calculation of WT. Quantitative assessment of contractile function by magnetic resonance (MR) tissue tagging and strain analysis may be less affected by these factors. METHODS: Two-dimensional regional WT and strain were calculated in three short-axis MR cine and tagged images, respectively. Left ventricular volumes and ejection fraction (EF) were obtained from a series of contiguous short-axis cine images. RESULTS: In patients with infarct-related ventricles, WT and strain analysis both revealed reduced myocardial function, as compared with control subjects (p < 0.005 and p < 0.001, respectively). However, WT analysis yielded no significant regional differences in function between infarct-related and remote myocardium (p = 0.064), whereas strain analysis did (p < 0.005). For detecting dysfunctional myocardium of electrocardiographically and angiographically defined infarct areas, WT analysis had a sensitivity of 69% and a specificity of 92%, whereas strain analysis demonstrated a sensitivity of 92% and a specificity of 99%. The EF correlated with WT (r = 0.76, p < 0.005) and strain (r = 0.89, p < 0.001). CONCLUSIONS: Two-dimensional strain analysis is more accurate than planar WT analysis in discriminating dysfunctional from functional myocardium, and it provides a strong correlation between regional myocardial and global ventricular function.
Magnetic resonance tagging has proven a valuable tool in the quantification of myocardial deformation. However, time-consuming postprocessing has discouraged the use of this technique in clinical routine. Recently, the harmonic phase (HARP) technique was introduced for automatic calculation of myocardial strain maps from tagged images. In this study, a comparison was made between HARP instantaneous strain maps calculated from single tagged images (SPAMM) and those calculated from subtracted tagged images (CSPAMM). The performance was quantified using simulated images of an incompressible cylinder in the 'end-systolic' state with realistic image contrast and noise. The error in the second principal stretch ratio was 0.009 +/- 0.032 (mean +/- SD) for the SPAMM acquisition, and 0.007 +/- 0.016 for CSPAMM at identical contrast-to-noise ratio. Furthermore, differences between the methods were illustrated with in vivo strain maps. Those calculated from CSPAMM images showed fewer artifacts and were less sensitive to the choice of cut-off frequencies in the HARP band-pass filter. A prerequisite for the method to become practical is that the CSPAMM images should be acquired in a single breathhold.
In a neonate born prior to term with a weight of 1825 grams, and diagnosed prenatally as having atrioventricular septal defect and Down's syndrome, we found the aortic arch to be interrupted between the left carotid artery and the left subclavian artery, with the arterial duct being the only route of distal perfusion. Three days later, however, echocardiographic interrogation revealed marked collateral connections between the aortic arch and the descending aorta, the picture then mimicking coarctation rather than interruption of the aortic arch. The rapid development of the collateral arteries was confirmed by magnetic resonance imaging and during cardiac surgery.
This study quantifies variance components of two-dimensional strains in the left-ventricular heart wall assessed by magnetic resonance (MR) tagging in 18 healthy xxvolunteers. For a 7-mm tagging grid and homogeneous strain analysis, the intersubject variability and measurement error were estimated, as well as the intra- and interobserver variability. The variance components were calculated for the mean strain of a circumferential sector. The results show that the measurement error was almost equal to the intra-observer variability. With four circumferential sectors of 90 degrees each, approximately 65% of the total variance in epsilonr and epsilonc was due to intersubject variability, the remaining 35% was due to measurement error. With 12 sectors of 30 degrees each, the intersubject variability and measurement error both contributed 50% to the total variance. With 18 sectors of 20 degrees each, only 40% of the total variance was due to intersubject variability. The total variability increased with the number of sectors and therefore the number of sectors used in a study will be a trade-off between segment size (defining spatial resolution) and variability.
Magnetic resonance (MR) flow mapping can be used to quantify flow velocity and volume flow in the coronary vessels noninvasively. The close anatomic relationship of the left anterior descending artery (LAD) with the great cardiac vein (GCV) allows imaging of both in one view. We examined the feasibility to discriminate between these two vessels based on the flow pattern and to measure the flow quantitatively. Eleven individuals with a normal LAD and 8 patients with a diseased LAD underwent MR imaging. From MR angiograms using connectivity to the aortic root, differentiation between the LAD and GCV was obtained. Perpendicular to both vessels, phase-contrast velocity mapping was performed to measure phasic and mean volume flow. After correction for cardiac motion of the vessel, GCV flow was found to be mainly systolic and pointing in the inverse direction as the predominantly diastolic flow in the LAD. These criteria appeared valid in all subjects, even in cases of highly stenotic arteries. The volume flow measurements corrected for body surface area were 31+/-15 ml/min/m2 in the normal LAD (n = 11) and 21+/-10 ml/min/m2 in the diseased LAD (n = 7). The volume flow measurements in the GCV corrected for body surface area were 23+/-19 ml/min/m2 in the normal vessels and 19+/-16 ml/min/m2 in the diseased vessels. In the patient with an occluded LAD and collaterals, the volume flow in the GCV was 7 ml/min/m2. MR is a unique tool for noninvasive simultaneous measurement of the flow pattern and volume flow in the GCV and the LAD, showing a clear distinction between arterial and venous flow.
The clinical value of magnetic resonance perfusion imaging (MRI) was investigated by quantitative comparison with (201)thallium-single-photon emission computed tomography ((201)TI-SPECT) and quantitative coronary angiography (QCA). Short-axis imaging was performed during dipyridamole administration in 13 patients with single-vessel coronary artery disease. Using inner and outer contours, the myocardium was divided into 30 contiguous, radial regions. Defining a perfusion defect as a region with less than 90% of maximum (201)TI intensity, nine patients had a matching perfusion defect, two had no defect on both (201)TI-SPECT or MRI, and one had a defect on (201)TI-SPECT but not on MRI. One patient had a defect on both modalities but with inaccurate localization. Three perfusion parameters were investigated: a) maximum contrast enhancement (MCE); b) slope of the signal intensity versus time curve; and c) inverse mean transit time (1/MTT). The sensitivity and specificity of MCE in the detection of perfusion abnormalities with TI-SPECT as the reference method were 71% and 71%, respectively (slope 77% and 61%, 1/MTT 44% and 70%). Furthermore, correlations were calculated per patient for the entire circumference of the short-axis myocardium. Median correlations were as follows: MCE 0.92, slope 0.91, and 1/MTT 0.40. Mismatches between (201)TI defects and defects on MRI resulted in low mean correlations (MCE 0.45, slope 0.46, and 1/MTT 0.26). There was a trend between severity of perfusion defects on MRI (using MCE) and QCA stenosis area (r = -0.56, P = 0.06). Thus, MRI and (201)TI-SPECT demonstrate fair agreement in the assessment of perfusion defects but show moderate correlation when the entire short-axis myocardium is correlated.
A robust algorithm to estimate three-dimensional strain in the left-ventricular heart wall, based on magnetic resonance (MR) grid-tagging in two sets of orthogonal image planes, is presented. Starting-point of this study was to minimize global interpolation and smoothing. Only the longitudinal displacement was interpolated between long-axis images. Homogeneous strain analysis was performed using small tetrahedrons. The method was tested using a stack of short-axis images and three long-axis images in six healthy volunteers. In addition, the method was subjected to an analytical test case, in which the effect of noise in tag point position on the observed strains was explored for normally distributed noise (0.5 mm RMS). In volunteers, the error in the longitudinal displacement due to interpolation between the long-axis image planes was -0.10 +/- 0. 48 mm (mean +/- SD). The resulting error in the longitudinal strain epsilon(l) was -0.003 +/- 0.02. The analytical test case was used to quantify the effects of three sources of errors on the observed strain. The SD of the difference between homogeneous strain and true strain was 0.06 for epsilon(r.) The error due to the 3-D reconstruction was 0.004 for epsilon(r.) The error in epsilon(r) resulting from simulated noise in the tag point position was 0.10. Equivalent results were obtained for all other strain parameters; thus, the error resulting from noise in the tag point position dominates the error introduced by approximations in the method. Because the proposed method uses a minimum of global interpolation and smoothing, it offers the prospect to detect small regions of aberrant contraction.
The purpose of the study was to investigate the potential of magnetic resonance imaging (MRI) to assess transmural differences in myocardial perfusion. Contrast-enhanced MRI was performed at rest and during hyperemia in a dog model and in 22 patients with single-vessel coronary artery disease. From MR signal intensity-versus-time curves, three perfusion parameters were derived: maximum myocardial contrast enhancement (MCE), slope, and inverse mean transit time (1/MTT). In dogs, MCE correlated well (r = 0.87, p < 0.00001) with microsphere-assessed myocardial blood flow. In the patients, the subendocardial MCE decreased during hyperemia (0.89 +/- 0.18 vs. 0.74 +/- 0.15, p < 0.003) and was lower in subendocardium than in subepicardium (0.74 +/- 0.15 vs. 0.84 +/- 0.21, p < 0.02). Parameters slope and 1/MTT paralleled MCE. Contrast-enhanced MRI reflects the transmural redistribution of myocardial perfusion during hyperemia. Perfusion abnormalities can be identified most distinctly in subendocardial myocardium.
A tracking algorithm was developed for calculation of three-dimensional point-specific myocardial motion. The algorithm was designed for images acquired with simultaneous magnetic resonance imaging (MRI) grid tagging and through-plane velocity quantification. The tagging grid provided the in-plane motion while the velocity quantification measured the through-plane motion. In four healthy volunteers, the in vivo performance was evaluated by comparing the systolic through-plane displacement with the displacement of tagging-grid intersections in long-axis images. The correlation coefficient was 0.93 (P < 0.001, N = 183). A t-test for paired samples revealed a small underestimation of the through-plane displacement by 0.04 +/- 0.09 cm (mean +/- SD, P < 0.001) on an average displacement of 0.77 +/- 0.23 cm toward the apex. The authors conclude that three-dimensional point-specific motion tracking based on simultaneous tagging and velocity quantification is competitive with other methods such as tagging in mutually orthogonal image planes or quantification of three orthogonal velocity components.
There is clear evidence in the literature that conventional spin-echo and gradient-echo magnetic resonance imaging (MRI) is capable of assessing patency of coronary artery vein grafts. With more recently introduced breath-hold two-dimensional (2D) and contrast-enhanced 3D techniques, the predictive accuracy has further improved, with sensitivities and specificities in the 90% range. Limitations arise with regard to assessing obstructive disease and evaluating distal segments of sequential grafts, due to insufficient spatial resolution, low signal-to-noise ratio, and cardiac motion. Imaging of arterial grafts is complicated by the metallic clip artifacts. Adding information on graft flow patterns and flow reserve using velocity-encoded cine MRI may help to reduce some of the problems. Clinically, these functional measurements may become of use in non-invasive monitoring of gradually increasing graft narrowing. However, apart from a few exceptions, most patients undergo evaluation of their grafts because they are considered for a re-intervention by angioplasty or coronary artery bypass graft surgery. In these cases information on the status of the native coronary arteries is required. A broader clinical use of MRI in the evaluation of patients with coronary artery bypass grafts may therefore only be expected with further improvement in MR techniques for coronary angiography. J. Magn. Reson. Imaging 1999;10:734-740.
BACKGROUND: After transmural myocardial infarction (MI), changes occur in intramural myocardial function. This has been described in anterior MI only. The aim of this study was to determine the relation between variable infarct locations and intramural deformation in patients with a first MI. METHODS: Forty patients (33 men and 7 women aged 57 +/- 11 years) with different infarct-related coronary arteries (25 left anterior descending, 7 circumflex, and 8 right coronary) were studied 6 +/- 3 days after infarction with magnetic resonance tissue tagging and 2-dimensional finite element analysis of myocardial deformation. Short-axis tagged images were acquired at base, mid, and apical level. Intramural deformation was measured in 6 circumferential segments per level. Results were compared with 9 age-matched healthy controls. RESULTS: Each infarct area demonstrated a significant reduction of intramural deformation. At mid-ventricular level, segments with maximum impaired intramural function were the anteroseptal segment for left anterior descending-related MI (stretch: 16% vs 33% for controls, P <.001), the posterolateral segment for related MI (stretch: 20% vs 34%, P <. 01); and the inferior segment for right coronary artery related MI (stretch: 18% vs 25%, P =.082). In these infarct segments, the intramural regional systolic stretch was more circumferentially oriented compared with radially oriented stretch in the same segments in controls (P <.05). CONCLUSION: The infarct area can be recognized by a specific spatial pattern of intramural deformation. In infarcted compared with noninfarcted myocardium, deformation is significantly reduced and systolic stretch deviates from the radial direction. Left anterior descending related infarcts were found to have larger regional differences in intramural deformation than circumflex or right coronary artery related MI of enzymatically the same size.