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Wesley D Gilson

Publications and source records attributed to Wesley D Gilson.

15 recordsLinked to original sources

Real-time imaging of regional myocardial function using fast-SENC.

A technique for fast imaging of regional myocardial function using a spiral acquisition in combination with strain-encoded (SENC) magnetic resonance imaging (MRI) is presented in this paper. This technique, which is termed fast-SENC, enables scan durations as short as a single heartbeat. A reduced field of view (FOV) without foldover artifacts was achieved by localized SENC, which selectively excited the region around the heart. The two images required for SENC imaging (low- and high-tuning) were acquired in an interleaved fashion throughout the cardiac cycle to further shorten the scan time. Regional circumferential contraction and longitudinal shortening of both the left ventricle (LV) and right ventricle (RV) were examined in long- and short-axis views, respectively. The in vivo results obtained from five human subjects and five infarcted dogs are presented. The results of the fast-SENC technique in a single heartbeat acquisition were comparable to those obtained by conventional SENC in a long acquisition time. Therefore, fast-SENC may prove useful for imaging during stress or arrhythmia.

Animals↗

Selective suppression of artifact-generating echoes in cine DENSE using through-plane dephasing.

In displacement-encoded imaging with stimulated echoes (DENSE), tissue displacement is encoded in the phase of the stimulated echo. However, three echoes generally contribute to the acquired signal (the stimulated echo, the complex conjugate of the stimulated echo, and an echo due to T(1) relaxation). It is usually desirable to suppress all except the stimulated echo, since otherwise the additional echoes will cause displacement measurement errors. Ideally, suppression of the artifact-generating echoes would be independent of time, T(1), and displacement-encoding frequency, and would not require additional acquisitions. In this study through-plane gradients were used to selectively dephase artifact-generating echoes without causing significant signal loss of the stimulated echo. A cine DENSE sequence was modified to include dephasing gradients and perform complementary spatial modulation of magnetization (CSPAMM). For single-acquisition cine DENSE using dephasing alone, artifact suppression was similar to CSPAMM with two acquisitions. The use of dephasing with CSPAMM required two acquisitions, but demonstrated greater artifact suppression than CSPAMM alone or dephasing alone.

Algorithms↗

Reperfused myocardial infarction in mice: 3D mapping of late gadolinium enhancement and strain.

We developed mathematical modeling tools for mapping 3D infarct geometry from multislice late gadolinium enhancement data, allowing fusion with multislice MR tagging data, in mice with myocardial infarction. Five C57BL/6 mice were imaged at baseline, 1, 7 and 28 days after 60 min occlusion of the left anterior descending coronary artery. The 3D infarct geometry was mapped in material coordinates, and registered with 3D strain, showing permanent dysfunction in infarcted segments, intermediate function in the adjacent zone, and maintained function in the remote zone. 3D mapping of late enhancement and strain allows registration of multiple studies in a consistent framework.

Analysis of Variance↗

Interaction between AT1 and AT2 receptors during postinfarction left ventricular remodeling.

The relative contribution of the angiotensin II type 1 and 2 receptors (AT1-R and AT2-R) in postmyocardial infarction (MI) remodeling remains incompletely understood. We studied five groups of C57Bl/6 mice after 1 h of left anterior descending artery occlusion-reperfusion: 1) wild type, untreated (n = 12); 2) wild type, treated with the AT1-R blocker losartan (10-20 mg.kg(-1).day(-1) in drinking water) from day 1 to day 28 post-MI (n = 10); 3) cardiac overexpression of the AT2-R [AT2-transgenic (TG); n = 14]; 4) AT2-TG treated with losartan (n = 13); and 5) AT2-TG and null for the AT1a-R [AT2-TG/AT1 knockout (KO); n = 10]. Cardiac magnetic resonance imaging (CMR) measured ejection fraction and left ventricular end-diastolic and end-systolic volume (EDVI and ESVI) and mass indexed to weight on days 0, 1, 7, and 28 post-MI. Infarct size was measured on day 1 by late gadolinium-enhanced CMR. Regional myocyte hypertrophy and collagen content were measured on day 28 post-MI. Infarct size was similar among groups. Systolic blood pressure was lowest in AT2-TG/AT1KO. By day 28 post-MI, when corrected for baseline differences, EDVI and ESVI were higher and ejection fraction was lower in wild type than other groups. Ejection fraction was highest and EDVI and mass index were lowest in AT2-TG/AT1KO at day 28. The AT2-TG/AT1KO demonstrated less fibrosis in adjacent regions. Regional myocyte hypertrophy was similar in all groups. The AT1-R and AT2-R are intricately intertwined in post-MI remodeling. Pharmacological blockade of AT1-R is equivalent to AT2-R overexpression in attenuating post-MI remodeling. Genetic knockout of the AT1a-R is additive to AT2-R overexpression, due, at least in part, to blood pressure lowering.

Animals↗

Dynamic imaging of allogeneic mesenchymal stem cells trafficking to myocardial infarction.

BACKGROUND: Recent results from animal studies suggest that stem cells may be able to home to sites of myocardial injury to assist in tissue regeneration. However, the histological interpretation of postmortem tissue, on which many of these studies are based, has recently been widely debated. METHODS AND RESULTS: With the use of the high sensitivity of a combined single-photon emission CT (SPECT)/CT scanner, the in vivo trafficking of allogeneic mesenchymal stem cells (MSCs) colabeled with a radiotracer and MR contrast agent to acute myocardial infarction was dynamically determined. Redistribution of the labeled MSCs after intravenous injection from initial localization in the lungs to nontarget organs such as the liver, kidney, and spleen was observed within 24 to 48 hours after injection. Focal and diffuse uptake of MSCs in the infarcted myocardium was already visible in SPECT/CT images in the first 24 hours after injection and persisted until 7 days after injection and was validated by tissue counts of radioactivity. In contrast, MRI was unable to demonstrate targeted cardiac localization of MSCs in part because of the lower sensitivity of MRI. CONCLUSIONS: Noninvasive radionuclide imaging is well suited to dynamically track the biodistribution and trafficking of mesenchymal stem cells to both target and nontarget organs.

Animals↗

The angiotensin II type 2 receptor and improved adjacent region function post-MI.

Angiotensin II type 2 receptor (AT2-R) overexpression in the mouse heart preserves left ventricular (LV) size and global LV function during post-MI remodeling. We hypothesized that CMR tagging would localize regional improvements in myocardial function during post-MI remodeling in AT2-R cardiac overexpressed transgenic mice (TG), which could explain the preservation of global LV function post-MI. Six male wild-type (WT) C57BL/6 mice and 10 TG mice were studied by CMR at baseline (day 0) and days 1, 7, and 28 post-MI. MI was induced by 1 hour occlusion of the LAD followed by reperfusion. On day 1 post-MI, gadolinium-DTPA was injected to assess infarct size. LV size and function was assessed by cine CMR. Mean % circumferential shortening (%CS) was calculated within infarcted, adjacent, and remote regions at each time point in WT and TG mice. Quantitative interstitial collagen and mean myocyte cross-sectional area was measured postmortem at day 28 post-MI. LV end-systolic volume was lower and ejection fraction higher at baseline in the TG group and these differences were maintained post-MI. Within infarcted and remote zones, although %CS was higher in TG mice at day 0, there was no difference by day 28 between groups. Within adjacent regions, while there was no difference at day 0 or 1 in TG vs. WT, %CS was significantly higher in TG mice by day 7, and these changes persisted out to day 28 post-MI. Regional interstitial collagen and myocyte size were similar between groups. Thus, myocardial tagging can detect regional differences in contractile function post-MI in TG mice, and AT2-R overexpression is associated with improved contractile function in adjacent noninfarcted myocardium.

Angiotensin II↗

Measurement of myocardial mechanics in mice before and after infarction using multislice displacement-encoded MRI with 3D motion encoding.

Cardiac MRI is an accurate, noninvasive modality for assessing the structure and function of the murine heart. In addition to conventional imaging, MRI tissue tracking methods can quantify numerous aspects of myocardial mechanics, including intramyocardial displacement, strain, twist, and torsion. In the present study, we developed and applied a novel pulse sequence based on displacement-encoded imaging using stimulated echoes (DENSE) that achieves multislice coverage, high spatial resolution, and three-dimensional (3D) displacement encoding. With the use of this technique, myocardial mechanics of C57Bl/6 mice were measured at baseline and 1 day after experimental myocardial infarction. At baseline, the mean systolic transmural circumferential strain was -0.14 +/- 0.02 and the mean systolic radial strain was 0.30 +/- 0.05. Changes in circumferential and radial strains from the subepicardium to the subendocardium were detected at baseline (P < 0.05). One day after infarction, significantly reduced 3D displacements and strain were detected in infarcted and noninfarcted myocardium. Infarction also reduced normalized systolic torsion from its baseline value of 1.35 +/- 0.27 degrees /mm (R = 0.99) to 0.07 +/- 0.54 degrees /mm (R = 0.96, P < 0.05). DENSE MRI can assess the 3D myocardial mechanics of the murine heart in <1 h of scan time at 4.7 T and may be applied to studies of myocardial mechanics in genetically engineered mice.

Animals↗

Simultaneous evaluation of infarct size and cardiac function in intact mice by contrast-enhanced cardiac magnetic resonance imaging reveals contractile dysfunction in noninfarcted regions early after myocardial infarction.

BACKGROUND: The objective of this study was to noninvasively determine the effects of reperfused myocardial infarction (MI) on regional and global left-ventricular (LV) function 24 hours after MI in intact mice with contrast-enhanced cardiac MRI and a single, gradient-echo pulse sequence. METHODS AND RESULTS: Twenty-three mice received baseline MRI scans followed by either 60 minutes of coronary occlusion (MI group, n=15) or thoracotomy without occlusion (sham group, n=8). Gadolinium-DTPA-enhanced magnetic resonance (MR) images were acquired 24 hours after surgery. Hearts were then excised for conventional infarct size determination via 2,3,5-triphenyl tetrazolium chloride (TTC) staining. In addition to infarct size, analysis of the MR images yielded left ventricular (LV) mass, LV end-systolic volume (LVESV), LV end-diastolic volume (LVEDV), LV ejection fraction (LVEF), cardiac output, and percent LV wall thickening (%WTh). Twenty-four hours after surgery, infarct size was 28.1+/-1.8% of LV mass by MRI and 27.5+/-1.7% by TTC (P=NS). Bland-Altman analysis revealed close agreement between the results obtained by the 2 methods. MI had little effect on LVEDV but caused a 98% increase in LVESV (from 11.3 to 22.4 microL, P<0.05), which resulted in a significant reduction in LVEF (from 70% to 37%, P<0.05). Compared with LV regional function at baseline, %WTh 24 hours after MI was significantly depressed, not only in infarcted myocardium but also in regions remote from the infarct zone. In contrast, sham-operated mice showed a small but significant increase in %WTh 24 hours after surgery (P<0.05). CONCLUSIONS: MRI can accurately assess both infarct size and cardiac function in intact mice early after large, reperfused MI, revealing the existence of contractile dysfunction in noninfarcted regions of the heart.

Animals↗

Myocardial tissue tracking with two-dimensional cine displacement-encoded MR imaging: development and initial evaluation.

A breath-hold two-dimensional cine magnetic resonance (MR) pulse sequence based on displacement encoding with stimulated echoes (DENSE) for quantitative myocardial motion tracking was developed and evaluated. In the sequence, complementary spatial modulation of magnetization was used for time-independent artifact suppression, and echo-planar imaging was used for rapid data sampling. Twelve healthy volunteers underwent cine DENSE MR imaging, and six of them also underwent conventional MR imaging myocardial tagging. The circumferential shortening component of strain (E(cc)) was measured on cine DENSE MR images and conventional tagged MR images. With complementary spatial modulation of magnetization, 10% or less of the total cine DENSE MR image energy was attributed to an artifact-generating echo during systolic imaging. Two-dimensional intramyocardial displacement and strain were measured at cine DENSE MR imaging with spatial resolution and temporal resolution of 2.7 x 2.7 mm and 60 msec, respectively. E(cc) measured at cine DENSE MR imaging correlated well with that measured at conventional MR imaging tagging (slope = 0.88, intercept = 0.00, R = 0.87).

Adult↗

Nitric oxide mediates benefits of angiotensin II type 2 receptor overexpression during post-infarct remodeling.

We hypothesized that nitric oxide (NO) mediates the benefits of cardiac angiotensin II type 2 (AT(2)-R) overexpression during postmyocardial infarction (post-MI) remodeling. Eleven wild-type (WT) C57BL/6 mice and 28 transgenic (TG) mice with AT(2)-R overexpression were studied by cardiac magnetic resonance imaging (CMR) at baseline and days 1 and 28 post-MI induced by left anterior descending artery occlusion and reperfusion. Sixteen TG mice were treated from day 1 through 28 post-MI with the NO synthase inhibitor N(G)-nitro-l-arginine methyl ester in drinking water at 1 mg/mL (TG-Rx). Left ventricular mass index (LVMI), end-diastolic volume index (EDVI) and end-systolic volume index (ESVI), wall thickness, percent thickening, and ejection fraction (EF) were measured. Infarct size on day 1 was assessed by post-contrast CMR. Interstitial collagen was quantified in noninfarcted regions. At baseline, heart rate (HR), blood pressure (BP), LVMI, EDVI, and ESVI were similar between groups, as were infarct size and weekly post-MI HR and systolic BP. By day 28 post-MI, EDVI and ESVI were similar in WT and TG-Rx, but significantly lower in TG (ESVI: 1.41+/-0.18 microL/g versus 2.53+/-0.14 microL/g in WT; 2.17+/-0.14 microL/g in TG-Rx; P<0.008 for both). At day 28, EF was higher in TG (46.3%+/-2.9%) compared with WT and TG-Rx (32.7+/-2.3% and 33.7+/-2.3, respectively; P<0.003 for both). Wall thickening at day 28 post-MI was greater in the base and mid-LV in TG than WT and TG-Rx. Noninfarcted region interstitial collagen was similar between groups. Thus, the NO pathway may mediate much of the benefits of cardiac AT(2)-R overexpression during post-MI remodeling.

Animals↗

Complementary displacement-encoded MRI for contrast-enhanced infarct detection and quantification of myocardial function in mice.

MRI is emerging as an important modality for assessing myocardial function in transgenic and knockout mouse models of cardiovascular disease, including myocardial infarction (MI). Displacement encoding with stimulated echoes (DENSE) measures myocardial motion at high spatial resolution using phase-reconstructed images. The current DENSE technique uses inversion recovery (IR) to suppress T(1)-relaxation artifacts; however, IR is ill-suited for contrast-enhanced infarct imaging in the heart, where multiple T(1) values are observed. We have developed a modified DENSE method employing complementary acquisitions for T(1)-independent artifact suppression. With this technique, displacement and strain are measured in phase-reconstructed images, and contrast-enhanced regions of infarction are depicted in perfectly coregistered magnitude-reconstructed images. The displacement measurements and T(1)-weighted image contrast were validated with the use of a rotating phantom. Modified DENSE was performed in mice (N = 9) before and after MI. Circumferential (E(cc)) and radial (E(rr)) strain were measured, and contrast-enhanced infarcted myocardium was detected by DENSE. At baseline, E(cc) was -0.16 +/- 0.01 and E(rr) was 0.39 +/- 0.07. After MI, E(cc) was 0.04 +/- 0.02 and E(rr) was 0.03 +/- 0.04 in infarcted regions, whereas E(cc) was -0.12 +/- 0.02 and E(rr) was 0.38 +/- 0.09 in noninfarcted regions. In vivo E(cc) as determined by DENSE correlated well with E(cc) obtained by conventional tag analysis (R = 0.90).

Animals↗

Increasing the signal-to-noise ratio in DENSE MRI by combining displacement-encoded echoes.

A new technique was developed to increase the signal-to-noise ratio (SNR) in displacement encoding with stimulated echoes (DENSE) MRI. This signal-averaged DENSE (sav-DENSE) technique is based on the SNR advantage of extracting a pair of DENSE images with uncorrelated noise from the complex complementary spatial modulation of the magnetization image, and combining them during image reconstruction. Eleven healthy volunteers were imaged at three short-axis locations with the use of sav-DENSE, cine DENSE, and myocardial tagging pulse sequences. In this study, sav-DENSE increased the SNR by 15-34% as compared to cine DENSE. Circumferential strain values measured by sav-DENSE and myocardial tagging were strongly correlated (slope = 0.95, intercept = -0.02, R = 0.92) and within the 95% limits of agreement. The breath-hold sav-DENSE technique yielded relatively accurate and precise quantification of 2D intramyocardial function, with a 40.2-ms temporal resolution and a 3.5 x 3.5 mm2 spatial resolution.

Adult↗

Displacement-encoded cardiac MRI using cosine and sine modulation to eliminate (CANSEL) artifact-generating echoes.

Displacement-encoded imaging with stimulated echoes (DENSE) and harmonic phase imaging (HARP) employ 1-1 spatial modulation of magnetization to cosine modulate the longitudinal magnetization as a function of position at end diastole. Later in the cardiac cycle they sample the cosine-modulated signal and compute myocardial strain from the signal phase. The sampled signal generally includes three distinct echoes: 1) a displacement-encoded stimulated echo, 2) the complex conjugate of the displacement-encoded echo, and 3) an echo arising from T1 relaxation. If the T1-relaxation and complex conjugate echoes are suppressed, then a phase image representing just the displacement-encoded echo can be reconstructed. In the present study, the use of cosine and sine modulation to eliminate (CANSEL) the T1-relaxation and complex conjugate echoes was investigated. With the use of CANSEL, it was demonstrated that DENSE accurately measures through-plane as well as in-plane components of tissue motion. Also, DENSE with CANSEL artifact suppression can provide increased signal-to-noise ratio (SNR) secondary to reduced intravoxel dephasing by using relatively low displacement-encoding frequencies. For applications that employ DENSE imaging with multiple acquisitions, the CANSEL technique can suppress artifact-generating echoes without placing constraints on the displacement-encoding frequency and direction.

Animals↗

Serial MRI evaluation of cardiac structure and function in mice after reperfused myocardial infarction.

This study evaluated the utility of cardiac MRI for assessing the impact of myocardial infarction (MI) on cardiac structure and function in mice following reperfused 1- or 2-hr occlusions of the left anterior descending coronary artery (LAD). When assessed 1 day after MI, the left ventricular ejection fraction (LVEF) had declined by more than half, and remained depressed for the duration of the study. Furthermore, MI initiated dramatic increases in both LV end-systolic volume (LVESV) and end-diastolic volume (LVEDV), with a greater than threefold increase in LVESV and a twofold increase in LVEDV by 4 weeks post-MI. Transmural LV wall thickening (WTh) analysis revealed that noninfarcted myocardium in the remote septal region exhibited an early deficit in contractile function after MI that transiently resolved by day 7, only to be followed by a late phase of dysfunction that became fully manifest by day 28 post-MI. In conclusion, MRI allows the serial assessment of cardiac structure and function after MI in mice, with a resolution adequate to document both regional and temporal changes. The application of these imaging techniques in transgenic and knock-out mice will greatly expedite research aimed at defining the functional roles of individual genes in the pathophysiology of LV remodeling (LVR) after reperfused MI.

Animals↗

MR tagging early after myocardial infarction in mice demonstrates contractile dysfunction in adjacent and remote regions.

The purpose of this study was to use MR myocardial tagging to assess regional cardiac function after myocardial infarction (MI) in mice. Eight mice were imaged before and 1 day after MI. MRI included cine imaging, myocardial tagging, and contrast-enhanced imaging. Regional percent circumferential shortening (%CS) was measured from the tagged images, and the region of hyperenhancement on the contrast-enhanced images was used to determine the infarcted, adjacent, and remote zones. Ejection fraction (EF) fell from 59% +/- 6% at baseline to 32% +/- 6% after MI (P < 0.01). At baseline, %CS was 14.5% +/- 3.4%. After MI, %CS was 0.7% +/- 4.4% in the infarcted zone, 7.4% +/- 4.4% in the adjacent zone, and 11.8% +/- 4.2% in the remote zone. %CS was statistically different for all comparisons between the infarcted, adjacent, remote, and baseline groups (P < 0.01). MR tagging can detect regional differences in myocardial function post-MI in mice.

Animals↗