Accurate grading of MR severity is crucial for appropriate patient management but remains challenging. VE-CMR with 3D three-directional acquisition has been recently proposed as the reference method.

A total of 64 patients with functional MR were included. A VE-CMR acquisition was applied to quantify mitral regurgitant volume (Rvol). Color Doppler 3D echocardiography was applied for direct measurement, in "en face" view, of mitral effective regurgitant orifice area (EROA); Rvol was subsequently calculated as EROA multiplied by the velocity-time integral of the regurgitant jet on the continuous-wave Doppler. To assess the relative potential error of the conventional approach, color Doppler 2-dimensional (2D) echocardiography was performed: vena contracta width was measured in the 4-chamber view and EROA calculated as circular (EROA-4CH); EROA was also calculated as elliptical (EROA-elliptical), measuring vena contracta also in the 2-chamber view. From these 2D measurements of EROA, the Rvols were also calculated.

The EROA measured by 3D echocardiography was significantly higher than EROA-4CH (p < 0.001) and EROA-elliptical (p < 0.001), with a significant bias between these measurements (0.10 cm² and 0.06 cm², respectively). Rvol measured by 3D echocardiography showed excellent correlation with Rvol measured by CMR (r = 0.94), without a significant difference between these techniques (mean difference = –0.08 ml/beat). Conversely, 2D echocardiographic approach from the 4-chamber view significantly underestimated Rvol (p = 0.006) as compared with CMR (mean difference = 2.9 ml/beat). The 2D elliptical approach demonstrated a better agreement with CMR (mean difference = –1.6 ml/beat, p = 0.04).

Quantification of EROA and Rvol of functional MR with 3D echocardiography is feasible and accurate as compared with VE-CMR; the currently recommended 2D echocardiographic approach significantly underestimates both EROA and Rvol.

Myocardial ischemic memory imaging, denoting the visualization of abnormalities provoked by ischemia and sustained even after restoration of perfusion, is desirable and allows after-the-fact recognition of ischemic insult. PST offers a sensitive marker of myocardial ischemia, but whether this abnormal thickening remains after relief from brief ischemia is unclear.

Tissue strain echocardiographic data were acquired from 27 dogs under 2 different conditions of myocardial ischemia induced by either brief coronary occlusion (15 or 5 min) followed by reperfusion (Protocol 1) or by dobutamine stress during nonflow-limiting stenosis (Protocol 2). Peak systolic strain and post-systolic strain index (PSI), a parameter of PST, were analyzed.

In Protocol 1, peak systolic strain was significantly decreased in the risk area during occlusion. This decrease in peak systolic strain in the 15-min group did not completely recover to baseline levels even 120 min after reperfusion, whereas the decrease in the 5-min group recovered immediately after reperfusion. We found that PSI was significantly increased during occlusion, but increased PSI in the 5-min group remained until 30 min after reperfusion (–0.19 ± 0.18 [baseline] vs. 0.19 ± 0.14 [30 min], p < 0.05) despite the rapid recovery of peak systolic strain. In Protocol 2, increased PSI was sustained until 20 min after the end of dobutamine infusion (–0.26 ± 0.11 [baseline] vs. –0.16 ± 0.10 [20 min], p < 0.05), although peak systolic strain recovered by 5 min after the end of dobutamine infusion.

PST remained longer than abnormal peak systolic strain after recovery from ischemia. Assessment of PST may be valuable for detecting myocardial ischemic memory.

Data on the progression of atherosclerosis stratified by plaque composition with the use of noninvasive assessment by CT are limited and hampered by high measurement variability.

This analysis included patients who presented with acute chest pain to the emergency department but initially showed no evidence of acute coronary syndromes. All patients underwent contrast-enhanced 64-slice CT at baseline and after 2 years with the use of a similar protocol. CT datasets were coregistered and assessed for the presence of calcified and noncalcified plaque at 1 mm cross sections of the proximal 40 mm of each major coronary artery. Plaque progression over time and its association with risk factors were determined. Measurement reproducibility and correlation to plaque volume was performed in a subset of patients.

We included 69 patients (mean age 55 ± 12 years, 59% male patients) and compared 8,311 coregistered cross sections at baseline and follow-up. At baseline, any plaque, calcified plaque, and noncalcified were detected in 12.5%, 10.1%, and 2.4% of cross sections per patient, respectively. There was significant progression in the mean number of cross sections containing any plaque (16.5 ± 25.3 vs. 18.6 ± 25.5, p = 0.01) and noncalcified plaque (3.1 ± 5.8 vs. 4.4 ± 7.0, p = 0.04) but not calcified plaque (13.3 ± 23.1 vs. 14.2 ± 22.0, p = 0.2). In longitudinal regression analysis, the presence of baseline plaque, number of cardiovascular risk factors, and smoking were independently associated with plaque progression after adjustment for age, sex, and follow-up time interval. The semiquantitative score based on cross sections correlated closely with plaque volume progression (r = 0.75, p < 0.0001) and demonstrated an excellent intraobserver and interobserver agreement ( = 0.95 and = 0.93, respectively).

Coronary plaque burden of patients with acute chest pain significantly increases during the course of 2 years. Progression over time is dependent on plaque composition and cardiovascular risk profile. Larger studies are needed to confirm these results and to determine the effect of medical treatment on progression.

An integrated approach to assess ventricular pump function, myocontractility (end-systolic pressure–volume relationship [ESPVR]), and diastolic compliance (end-diastolic pressure–volume relation [EDPVR]) is of high clinical value. Cardiac magnetic resonance (CMR) is well established for measuring global pump function, and catheterization-combined CMR was previously shown to accurately measure ESPVR, but not yet the EDPVR.

In 8 pigs, the CMR technique was compared with conductance catheter methods (gold standard) for measuring the EDPVR in the left and right ventricle. Measurements were performed at rest and during dobutamine administration. For CMR, the ESPVR was estimated with a single-beat approach by synchronizing invasive ventricular pressures with cine CMR–derived ventricular volumes. The EDPVR was determined during pre-load reduction from additional volume data that were obtained from real-time velocity-encoded CMR pulmonary/aortic blood flow measurements. Pre-load reduction was achieved by transient balloon occlusion of the inferior vena cava. The stiffness coefficient β was calculated by an exponential fit from the EDPVR. After validation in the animal experiments, the EDPVR was assessed in a pilot study of 3 patients with a single ventricle using identical CMR and conductance catheter techniques.

Bland-Altman tests showed good agreement between conductance catheter–derived and CMR-derived EDPVR. In both ventricles of the pigs, dobutamine enhanced myocontractility (p < 0.01), increased stroke volume (p < 0.01), and improved diastolic function. The latter was evidenced by shorter early relaxation (p < 0.05), a downward shift of the EDPVR, and a decreased stiffness coefficient β (p < 0.05). In contrast, in the patients, early relaxation was inconspicuous but the EDPVR shifted left-upward and the stiffness constant remained unchanged. The observed changes in diastolic function were not significantly different when measured with conductance catheter and CMR.

This novel CMR method provides differential information about diastolic function in conjunction with parameters of systolic contractility and global pump function.

Patients with an unrestricted left-to-right shunt who are at risk of obstructive pulmonary vascular disease require PVR evaluation preoperatively. CMR cardiac catheter (XMR) combines noninvasive measurement of Qp by phase contrast imaging with invasive pressure measurement to accurately determine the PVR.

Patients referred for clinical assessment of the PVR were included. The XMR was used to determine the PVR. The noninvasive parameters, Qp and left-to-right shunt (Qp/Qs), were compared with the PVR using univariate regression models.

The XMR was undertaken in 26 patients (median age 0.87 years)—ventricular septal defect 46.2%, atrioventricular septal defect 42.3%. Mean aortic flow was 2.24 ± 0.59 l/min/m², and mean Qp was 6.25 ± 2.78 l/min/m². Mean Qp/Qs was 2.77 ± 1.02. Mean pulmonary artery pressure was 34.8 ± 10.9 mm Hg. Mean/median PVR was 5.5/3.0 Woods Units (WU)/m² (range 1.7 to 31.4 WU/m²). The PVR was related to both Qp and Qp/Qs in an inverse exponential fashion by the univariate regression equations PVR = exp(2.53 – 0.20[Qp]) and PVR = exp(2.75 – 0.52[Qp/Qs]). Receiver-operator characteristic (ROC) analysis was used to determine cutoff values for Qp and Qp/Qs above which the PVR could be regarded as clinically acceptable. A Qp of ≥6.05 l/min/m² predicted a PVR of ≤3.5 WU/m² with sensitivity 72%, specificity 100%, and area under the ROC curve 0.90 (p = 0.002). A Qp/Qs of ≥2.5/1 predicted a PVR of ≤3.5 WU/m² with sensitivity 83%, specificity 100%, and area under the curve ROC 0.94 (p < 0.001).

Measurement of Qp or left-to-right shunt noninvasively by CMR has potential to predict the PVR in patients with an unrestricted left-to-right shunt and could potentially determine operability without having to undertake invasive testing.

CMR is suitable for diagnosing inducible myocardial ischemia in patients with suspected CAD and has been proven to be a helpful diagnostic tool for decision of further treatment. However, little is known about its diagnostic accuracy in patients with known CAD who previously were treated by PCI or CABG.

A total of 477 patients with suspected CAD, 236 with previous PCI, and 110 after CABG referred for coronary X-ray angiography (CXA) underwent an integrated CMR examination before CXA. Myocardial ischemia was assessed using first-pass perfusion after vasodilator stress with adenosine (140 µg/kg/min for 3 min) using gadolinium-based contrast agents (0.1 mmol/kg). Late gadolinium enhancement (LGE) was assessed 10 min after a second contrast bolus.

CXA demonstrated a relevant coronary vessel stenosis (≥70% luminal reduction) in 313 (38%) patients using quantitative coronary analysis. The combination of CMR perfusion and LGE assessment for detecting a relevant coronary stenosis in patients with suspected CAD yielded sensitivity and specificity of 0.94 and 0.87, in PCI patients 0.91 and 0.90, and in CABG patients 0.79 and 0.77, respectively.

A combined CMR protocol for the assessment of myocardial perfusion and LGE is feasible for the detection of relevant coronary vessel stenosis even in patients who previously were treated by PCI or CAG in a routine clinical setting. However, diagnostic accuracy is reduced in patients with CABG. This could be due to different flow and perfusion kinetic. Further studies are needed to optimize the clinical protocols especially in post-surgical patients.

Myocardial ischemia enhances late sodium current, which then causes cellular calcium overload leading to mechanical left ventricular dysfunction and arrhythmias. Ranolazine inhibits late sodium current and improves diastolic tension and MBF in the animal model.

In this open-label, nonrandomized pilot study, we recruited 20 patients with known or a high probability of CAD and who had reversible perfusion defects on exercise treadmill gated single-photon emission computed tomography MPI while receiving conventional antianginal therapy. Ranolazine (up to 1,000 mg twice daily) was added to baseline therapy and a repeat treadmill MPI was obtained after 4 weeks. The extent and severity of total and reversible left ventricular perfusion abnormality (based on polar maps and a 17-segment model) were determined quantitatively using automated methods.

We screened 100 patients for 27 potential candidates; 5 declined and 2 did not complete the follow-up study. The mean age of the remaining 20 patients was 64 ± 9 years; 30% were women and 50% had diabetes mellitus. The exercise time increased (425 ± 105 s vs. 393 ± 116 s, p = 0.017), and angina improved in 15 (75%) patients after ranolazine treatment. In the entire cohort, summed stress scores (10 ± 7 vs. 13 ± 8, p = 0.04) and summed difference scores (4.7 ± 4 vs. 7.4 ± 5, p = 0.0037) decreased at follow-up. An improvement in perfusion pattern and severity was noted in 14 (70%) patients. In these patients, the polar maps showed a decrease in total abnormality from 26 ± 17% to 19 ± 15% and a decrease in the reversible abnormality from 16 ± 10% to 8 ± 6% (all p values <0.05).

In this preliminary hypothesis-driven study, short-term ranolazine therapy was shown to improve myocardial perfusion and decrease the ischemic burden in patients with CAD.