Joel R Wilson

Extracellular volume fraction mapping in the myocardium, part 1: evaluation of an automated method

BackgroundDisturbances in the myocardial extracellular volume fraction (ECV), such as diffuse or focal myocardial fibrosis or edema, are hallmarks of heart disease. Diffuse ECV changes are difficult to assess or quantify with cardiovascular magnetic resonance (CMR) using conventional late gadolinium enhancement (LGE), or pre- or post-contrast T1-mapping alone. ECV measurement circumvents factors that confound T1-weighted images or T1-maps, and has been shown to correlate well with diffuse myocardial fibrosis. The goal of this study was to develop and evaluate an automated method for producing a pixel-wise map of ECV that would be adequately robust for clinical work flow.MethodsECV maps were automatically generated from T1-maps acquired pre- and post-contrast calibrated by blood hematocrit. The algorithm incorporates correction of respiratory motion that occurs due to insufficient breath-holding and due to misregistration between breath-holds, as well as automated identification of the blood pool. Images were visually scored on a 5-point scale from non-diagnostic (1) to excellent (5).ResultsThe quality score of ECV maps was 4.23 ± 0.83 (m ± SD), scored for n = 600 maps from 338 patients with 83% either excellent or good. Co-registration of the pre-and post-contrast images improved the image quality for ECV maps in 81% of the cases. ECV of normal myocardium was 25.4 ± 2.5% (m ± SD) using motion correction and co-registration values and was 31.5 ± 8.7% without motion correction and co-registration.ConclusionsFully automated motion correction and co-registration of breath-holds significantly improve the quality of ECV maps, thus making the generation of ECV-maps feasible for clinical work flow.

Extracellular volume fraction mapping in the myocardium, part 2: initial clinical experience

BackgroundDiffuse myocardial fibrosis, and to a lesser extent global myocardial edema, are important processes in heart disease which are difficult to assess or quantify with cardiovascular magnetic resonance (CMR) using conventional late gadolinium enhancement (LGE) or T1-mapping. Measurement of the myocardial extracellular volume fraction (ECV) circumvents factors that confound T1-weighted images or T1-maps. We hypothesized that quantitative assessment of myocardial ECV would be clinically useful for detecting both focal and diffuse myocardial abnormalities in a variety of common and uncommon heart diseases.MethodsA total of 156 subjects were imaged including 62 with normal findings, 33 patients with chronic myocardial infarction (MI), 33 with hypertrophic cardiomyopathy (HCM), 15 with non-ischemic dilated cardiomyopathy (DCM), 7 with acute myocarditis, 4 with cardiac amyloidosis, and 2 with systemic capillary leak syndrome (SCLS). Motion corrected ECV maps were generated automatically from T1-maps acquired pre- and post-contrast calibrated by blood hematocrit. Abnormally-elevated ECV was defined as >2SD from the mean ECV in individuals with normal findings. In HCM the size of regions of LGE was quantified as the region >2 SD from remote.ResultsMean ECV of 62 normal individuals was 25.4 ± 2.5% (m ± SD), normal range 20.4%-30.4%. Mean ECV within the core of chronic myocardial infarctions (without MVO) (N = 33) measured 68.5 ± 8.6% (p < 0.001 vs normal). In HCM, the extent of abnormally elevated ECV correlated to the extent of LGE (r = 0.72, p < 0.001) but had a systematically greater extent by ECV (mean difference 19 ± 7% of slice). Abnormally elevated ECV was identified in 4 of 16 patients with non-ischemic DCM (38.1 ± 1.9% (p < 0.001 vs normal) and LGE in the same slice appeared “normal” in 2 of these 4 patients. Mean ECV values in other disease entities ranged 32-60% for cardiac amyloidosis (N = 4), 40-41% for systemic capillary leak syndrome (N = 2), and 39-56% within abnormal regions affected by myocarditis (N = 7).ConclusionsECV mapping appears promising to complement LGE imaging in cases of more homogenously diffuse disease. The ability to display ECV maps in units that are physiologically intuitive and may be interpreted on an absolute scale offers the potential for detection of diffuse disease and measurement of the extent and severity of abnormal regions.

MultiContrast Delayed Enhancement (MCODE) improves detection of subendocardial myocardial infarction by late gadolinium enhancement cardiovascular magnetic resonance: a clinical validation study.

BackgroundMyocardial infarction (MI) documented by late gadolinium enhancement (LGE) has clinical and prognostic importance, but its detection is sometimes compromised by poor contrast between blood and MI. MultiContrast Delayed Enhancement (MCODE) is a technique that helps discriminate subendocardial MI from blood pool by simultaneously providing a T2-weighted image with a PSIR (phase sensitive inversion recovery) LGE image. In this clinical validation study, our goal was to prospectively compare standard LGE imaging to MCODE in the detection of MI.MethodsImaging was performed on a 1.5 T scanner on patients referred for CMR including a LGE study. Prospective comparisons between MCODE and standard PSIR LGE imaging were done by targeted, repeat imaging of slice locations. Clinical data were used to determine MI status. Images at each of multiple time points were read on separate days and categorized as to whether or not MI was present and whether an infarction was transmural or subendocardial. The extent of infarction was scored on a sector-by-sector basis.ResultsSeventy-three patients were imaged with the specified protocol. The majority were referred for vasodilator perfusion exams and viability assessment (37 ischemia assessment, 12 acute MI, 10 chronic MI, 12 other diagnoses). Forty-six patients had a final diagnosis of MI (30 subendocardial and 16 transmural). MCODE had similar specificity compared to LGE at all time points but demonstrated better sensitivity compared to LGE performed early and immediately before and after the MCODE (p = 0.008 and 0.02 respectively). Conventional LGE only missed cases of subendocardial MI. Both LGE and MCODE identified all transmural MI. Based on clinical determination of MI, MCODE had three false positive MI’s; LGE had two false positive MI’s including two of the three MCODE false positives. On a per sector basis, MCODE identified more infarcted sectors compared to LGE performed immediately prior to MCODE (p < 0.001).ConclusionWhile both PSIR LGE and MCODE were good in identifying MI, MCODE demonstrated more subendocardial MI’s than LGE and identified a larger number of infarcted sectors. The simultaneous acquisition of T1 and T2-weighted images improved differentiation of blood pool from enhanced subendocardial MI.

Safety and tolerability of regadenoson CMR.

Aims Knowledge of adverse events associated with regadenoson perfusion cardiac magnetic resonance (CMR) and patient tolerability has implications for patient safety and staff training. We sought to assess the safety and tolerability of regadenoson stress CMR. Materials and methods A group of 728 consecutive patients (median age 58, 44% female) and 25 normal volunteers (median age 21, 24% female) were recruited from August 2009 to March 2012 using a prospective, cross-sectional study design. Subjects were stressed using fixed-dose regadenoson and imaged using a 1.5T MRI scanner. Symptoms and adverse events including death, myocardial infarction (MI), ventricular tachycardia (VT)/ventricular fibrillation (VF), hospitalization, arrhythmias, and haemodynamic stability were assessed. Results There were no occurrences of death, MI, VT/VF, high-grade atrioventricular block, or stress-induced atrial fibrillation. Notable adverse events included one case of bronchospasm and one case of heart failure exacerbation resulting in hospitalization. The most common symptoms in patients were dyspnoea (30%, n = 217), chest discomfort (27%, n = 200), and headache (15%, n = 111). There was minimal change between baseline and peak systolic and diastolic blood pressure in both patients and volunteers (P > 0.05). A blunted heart rate response to regadenoson was noted in patients with body mass index (BMI) ≥30 kg/m2 (P < 0.001), and diabetes (P = 0.001). Conclusions Regadenoson CMR is well tolerated and can be performed safely with few adverse events.

Transthoracic delivery of large devices into the left ventricle through the right ventricle and interventricular septum: preclinical feasibility

BackgroundWe aim to deliver large appliances into the left ventricle through the right ventricle and across the interventricular septum. This transthoracic access route exploits immediate recoil of the septum, and lower transmyocardial pressure gradient across the right versus left ventricular free wall. The route may enhance safety and allow subxiphoid rather than intercostal traversal.MethodsThe entire procedure was performed under real-time CMR guidance. An “active” CMR needle crossed the chest, right ventricular free wall, and then the interventricular septum to deliver a guidewire then used to deliver an 18Fr introducer. Afterwards, the right ventricular free wall was closed with a nitinol occluder. Immediate closure and late healing of the unrepaired septum and free wall were assessed by oximetry, angiography, CMR, and necropsy up to four weeks afterwards.ResultsThe procedure was successful in 9 of 11 pigs. One failed because of refractory ventricular fibrillation upon needle entry, and the other because of inadequate guidewire support. In all ten attempts, the right ventricular free wall was closed without hemopericardium. There was neither immediate nor late shunt on oximetry, X-ray angiography, or CMR. The interventricular septal tract fibrosed completely. Transventricular trajectories planned on human CT scans suggest comparable intracavitary working space and less acute entry angles than a conventional atrial transseptal approach.ConclusionLarge closed-chest access ports can be introduced across the right ventricular free wall and interventricular septum into the left ventricle. The septum recoils immediately and heals completely without repair. A nitinol occluder immediately seals the right ventricular wall. The entry angle is more favorable to introduce, for example, prosthetic mitral valves than a conventional atrial transseptal approach.

Transposition of Great Arteries

Transposition of the great arteries (TGA) is a form of conotruncal abnormalities in which the aorta arises from the morphological right ventricle and pulmonary artery arises from the morphological left ventricle (ventriculoarterial discordance). TGA encompasses two distinct defects, complete TGA and congenitally corrected TGA. Complete TGA has a prevalence of 0.24/1,000 live births [12] and represents ∼% of all congenital heart disease [25]. It is the second most common congenital heart defect recognized in infancy [12]. Congenitally corrected TGA is rarer, recognized in 0.02–0.07 per 1,000 live births [15], or less than 1 % of congenital heart defects [25].

Multimodality Imaging of a Dissecting Intramyocardial Hematoma Extending into the Left Atrial Wall Following Myocardial Infarction

Five days after the onset of substernal chest pain, a 60-year-old man with a history of hypertension, smoking (60 pack-years), severe bullous emphysema, and epilepsy presented with acutely worsening chest pain. Pharmacological management for non–ST-segment elevation myocardial infarction was initiated based on 12-lead ECG findings of subtle anterolateral ST segment changes (V2–V5) and a troponin I level of 6.36 ng/mL (normal <0.04 ng/mL). Invasive angiography demonstrated a distal occlusion of a right posterolateral branch and a nonocclusive stenosis in the distal circumflex artery (Figure 1A and ⇓B). Cineangiography showed two small craters of contrast protruding outside the contrast-filled left ventricular contour within a dyskinetic basal inferior wall (Figure 1C and ⇓D and online-only Data Supplement Movie I). Because the occlusion was distal, percutaneous coronary intervention was not performed. Transthoracic echocardiography showed heterogeneous echogenicity within a 28-mm-thick, dyskinetic, inferior left ventricular wall (online-only Data Supplement Movie II) and a mass protruding into the left atrium (Figure 2). This unusual mass was suspicious for an intramyocardial hematoma based on the clinical setting and its location within myocardium subtended by the occluded artery. Left ventricular ejection fraction was estimated visually to be 45%. There were wall motion abnormalities in the basal and midanterolateral, inferolateral, and inferior walls extending into the apical inferior wall. In retrospect, the anterolateral ST changes likely represented a combination of inferior and inferolateral infarct and ischemia. All antiplatelet and …

Time resolved measure of coronary sinus flow following regadenoson administration

Objective To use velocity encoded phase contrast MRI to determine timing of peak myocardial blood flow to establish when CMR stress perfusion imaging should be performed after injection of regadenoson.

Regadenoson is a better myocardial vasodilator than dipyridamole in normal volunteers, but the data is less compelling in patients

Regadenoson is a selective Adenosine-2A receptor agonist and is used for myocardial perfusion imaging. Dipyridamole causes indirect vasodilation by inhibiting cellular reuptake of adenosine. The purpose of this study was to assess whether regadenoson is a better coronary vasodilator than dipyridamole in normal volunteers and in patients.

Optimal timing of rest perfusion with regadenoson stress testing - normal volunteer study of quantitative MRI perfusion

Many MRI perfusion protocols perform rest imaging a few minutes after stress imaging. Regadenoson is a new, selective Adenosine-2A receptor agonist used for myocardial perfusion imaging. The purpose of this study was to assess how well rest perfusion imaging 20 minutes after regadenoson stress reflects true baseline rest perfusion.