Objectives To assess the relationship between extracellular volume (ECV), native T1, and systolic strain in hypertensive patients with left ventricular hypertrophy (HTN LVH), hypertensive patients without LVH (HTN Non-LVH) and normotensive controls. Background Diffuse myocardial fibrosis in HTN LVH patients, as reflected by increased ECV and native T1, may be an underlying mechanism contributing to increased cardiovascular risk when compared to HTN Non-LVH subjects and controls. Furthermore increased diffuse fibrosis in HTN LVH subjects may be associated with reduced peak systolic and early diastolic strain rate when compared to the other two groups. Methods T1 mapping was performed in 20 HTN LVH (55±11 years), 23 HTN Non-LVH (61±12) and 22 control (54±7) subjects on a Siemens 1.5T Avanto using a previously validated MOLLI pulse sequence. T1 was measured pre-contrast and 10, 15 and 20 minutes following injection of 0.15 mmol/kg Gd-DTPA, and the mean ECV and native T1 were determined for each subject. Measurement of circumferential strain parameters were performed using cine displacement encoding with stimulated echoes (DENSE). Results HTN LVH subjects had higher native T1 when compared to controls (p < 0.05). HTN LVH subjects had higher ECV when compared to HTN Non-LVH subjects and controls (p < 0.05). Peak systolic circumferential strain and early diastolic strain rate were reduced in HTN LVH subjects when compared to HTN Non-LVH subjects and controls (p < 0.05). Increased levels of ECV and Native T1 were associated with reduced peak systolic and early diastolic circumferential strain rate across all subjects. Conclusions HTN LVH patients had higher ECV, longer native T1 and associated reduction in peak systolic circumferential strain and early diastolic strain rate when compared to HTN Non-LVH and control subjects. Measurement of ECV and native T1 provide a non-invasive assessment of diffuse fibrosis in hypertensive heart disease.

Loss of beta-cell function in type 1 and type 2 diabetes leads to metabolic dysregulation and inability to maintain normoglycemia. Noninvasive imaging of beta-cell function in vivo would therefore provide a valuable diagnostic and research tool for quantifying progression to diabetes and response to therapeutic intervention. Because manganese (Mn(2+)) is a longitudinal relaxation time (T1)-shortening magnetic resonance imaging (MRI) contrast agent that enters cells such as pancreatic beta-cells through voltage-gated calcium channels, we hypothesized that Mn(2+)-enhanced MRI of the pancreas after glucose infusion would allow for noninvasive detection of beta-cell function in vivo. To test this hypothesis, we administered glucose and saline challenges intravenously to normal mice and mice given high or low doses of streptozotocin (STZ) to induce diabetes. Serial inversion recovery MRI was subsequently performed after Mn(2+) injection to probe Mn(2+) accumulation in the pancreas. Time-intensity curves of the pancreas (normalized to the liver) fit to a sigmoid function showed a 51% increase in signal plateau height after glucose stimulation relative to saline (P < 0.01) in normal mice. In diabetic mice given a high dose of STZ, only a 9% increase in plateau signal intensity was observed after glucose challenge (P = not significant); in mice given a low dose of STZ, a 20% increase in plateau signal intensity was seen after glucose challenge (P = 0.02). Consistent with these imaging findings, the pancreatic insulin content of high- and low-dose STZ diabetic mice was reduced about 20-fold and 10-fold, respectively, compared with normal mice. We conclude that Mn(2+)-enhanced MRI demonstrates excellent potential as a means for noninvasively monitoring beta-cell function in vivo and may have the sensitivity to detect progressive decreases in function that occur in the diabetic disease process.

Objectives The purpose of this paper was to compare quantitative cardiac magnetic resonance (CMR) first-pass contrast-enhanced perfusion imaging to qualitative interpretation for determining the presence and severity of coronary artery disease (CAD). Background Adenosine CMR can detect CAD by measuring perfusion reserve (PR) or by qualitative interpretation (QI). Methods Forty-one patients with an abnormal nuclear stress scheduled for X-ray angiography underwent dual-bolus adenosine CMR. Segmental myocardial perfusion analyzed using both QI and PR by Fermi function deconvolution was compared to quantitative coronary angiography. Results In the 30 patients with complete quantitative data, PR (mean ± SD) decreased stepwise as coronary artery stenosis (CAS) severity increased: 2.42 ± 0.94 for <50%, 2.14 ± 0.87 for 50% to 70%, and 1.85 ± 0.77 for > 70% (p < 0.001). The PR and QI had similar diagnostic accuracies for detection of CAS > 50% (83% vs. 80%), and CAS > 70% (77% vs. 67%). Agreement between observers was higher for quantitative analysis than for qualitative analysis. Using PR, patients with triple-vessel CAD had a higher burden of detectable ischemia than patients with single-vessel CAD (60% vs. 25%; p = 0.02), whereas no difference was detected by QI (31% vs. 21%; p = 0.26). In segments with myocardial scar (n = 64), PR was 3.10 ± 1.34 for patients with CAS <50% (n = 18) and 1.91 ± 0.96 for CAS >50% (p < 0.0001). Conclusions Quantitative PR by CMR differentiates moderate from severe stenoses in patients with known or suspected CAD. The PR analysis differentiates triple- from single-vessel CAD, whereas QI does not, and determines the severity of CAS subtending myocardial scar. This has important implications for assessment of prognosis and therapeutic decision making.

Background Gene-modified mice may be used to elucidate molecular mechanisms underlying abnormal myocardial blood flow (MBF). We sought to develop a quantitative myocardial perfusion imaging technique for mice and to test the hypothesis that myocardial perfusion reserve (MPR) is reduced in a mouse model of diet-induced obesity (DIO). Methods A dual-contrast saturation-recovery sequence with ky-t undersampling and a motion-compensated compressed sensing reconstruction algorithm was developed for first-pass MRI on a small-bore 7T system. Control mice were imaged at rest and with the vasodilators ATL313 and Regadenoson (n=6 each). In addition, we imaged mice fed a high-fat diet (HFD) for 24 weeks. Results In control mice, MBF was 5.7±0.8 ml/g/min at rest and it increased to 11.8±0.6 ml/g/min with ATL313 and to 10.4±0.3 ml/g/min with Regadenoson. In HFD mice we detected normal resting MBF (5.6±0.4 vs. 5.0±0.3 on control diet), low MBF at stress (7.7±0.4 vs. 10.4±0.3 on control diet, p<0.05), and reduced MPR (1.4±0.2 vs. 2.0±0.3 on control diet, p<0.05). Conclusions Accelerated dual-contrast first-pass MRI with motion-compensated compressed sensing provides spatiotemporal resolution suitable for measuring MBF in free-breathing mice, and detected reduced MPR in DIO mice. These techniques may be used to study molecular mechanisms that underlie abnormal myocardial perfusion.