Graham J. Fent

Acute Infarct Extracellular Volume Mapping to Quantify Myocardial Area at Risk and Chronic Infarct Size on Cardiovascular Magnetic Resonance ImagingCLINICAL PERSPECTIVE

Background— Late gadolinium enhancement (LGE) imaging overestimates acute infarct size. The main aim of this study was to investigate whether acute extracellular volume (ECV) maps can reliably quantify myocardial area at risk (AAR) and final infarct size (IS). Methods and Results— Fifty patients underwent cardiovascular magnetic resonance imaging acutely (24–72 hours) and at convalescence (3 months). The cardiovascular magnetic resonance protocol included cines, T2-weighted imaging, native T1 maps, 15-minute post-contrast T1 maps, and LGE. Optimal AAR and IS ECV thresholds were derived in a validation group of 10 cases (160 segments). Eight hundred segments (16 per patient) were analyzed to quantify AAR/IS by ECV maps (ECV thresholds for AAR is 33% and IS is 46%), T2-weighted imaging, T1 maps, and acute LGE. Follow-up LGE imaging was used as the reference standard for final IS and viability assessment. The AAR derived from ECV maps (threshold of >33) demonstrated good agreement with T2-weighted imaging–derived AAR (bias, 0.18; 95% confidence interval [CI], −1.6 to 1.3) and AAR derived from native T1 maps (bias=1; 95% CI, −0.37 to 2.4). ECV demonstrated the best linear correlation to final IS at a threshold of >46% (R=0.96; 95% CI, 0.92–0.98; P<0.0001). ECV maps demonstrated better agreement with final IS than acute IS on LGE (ECV maps: bias, 1.9; 95% CI, 0.4–3.4 versus LGE imaging: bias, 10; 95% CI, 7.7–12.4). On multiple variable regression analysis, the number of nonviable segments was independently associated with IS by ECV maps (&bgr;=0.86; P<0.0001). Conclusions— ECV maps can reliably quantify AAR and final IS in reperfused acute myocardial infarction. Acute ECV maps were superior to acute LGE in terms of agreement with final IS. IS quantified by ECV maps are independently associated with viability at follow-up.

The role of non-invasive cardiovascular imaging in the assessment of cardiovascular risk in rheumatoid arthritis: where we are and where we need to be

This review assesses the risk assessment of cardiovascular disease (CVD) in rheumatoid arthritis (RA) and how non-invasive imaging modalities may improve risk stratification in future. RA is common and patients are at greater risk of CVD than the general population. Cardiovascular (CV) risk stratification is recommended in European guidelines for patients at high and very high CV risk in order to commence preventative therapy. Ideally, such an assessment should be carried out immediately after diagnosis and as part of ongoing long-term patient care in order to improve patient outcomes. The risk profile in RA is different from the general population and is not well estimated using conventional clinical CVD risk algorithms, particularly in patients estimated as intermediate CVD risk. Non-invasive imaging techniques may therefore play an important role in improving risk assessment. However, there are currently very limited prognostic data specific to patients with RA to guide clinicians in risk stratification using these imaging techniques. RA is associated with increased risk of CV mortality, mainly attributable to atherosclerotic disease, though in addition, RA is associated with many other disease processes which further contribute to increased CV mortality. There is reasonable evidence for using carotid ultrasound in patients estimated to be at intermediate risk of CV mortality using clinical CVD risk algorithms. Newer imaging techniques such as cardiovascular magnetic resonance and CT offer the potential to improve risk stratification further; however, longitudinal data with hard CVD outcomes are currently lacking.

Comparison of fast acquisition strategies in whole‐heart four‐dimensional flow cardiac MR: Two‐center, 1.5 Tesla, phantom and in vivo validation study

To validate three widely‐used acceleration methods in four‐dimensional (4D) flow cardiac MR; segmented 4D‐spoiled‐gradient‐echo (4D‐SPGR), 4D‐echo‐planar‐imaging (4D‐EPI), and 4D‐k‐t Broad‐use Linear Acquisition Speed‐up Technique (4D‐k‐t BLAST).

A Novel and Practical Screening Tool for the Detection of Silent Myocardial Infarction in Patients With Type 2 Diabetes

Objective: Silent myocardial infarction (MI) is a prevalent finding in patients with type 2 diabetes and is associated with significant mortality and morbidity. Late gadolinium enhancement (LGE) by cardiovascular magnetic resonance (CMR) is the most validated technique for detection of silent MI, but is time-consuming, costly, and requires administration of intravenous contrast. We therefore planned to develop a simple and low-cost population screening tool to identify those at highest risk of silent MI validated against the CMR reference standard. Methods: A total of 100 asymptomatic patients with type 2 diabetes underwent electrocardiogram (ECG), echocardiography, biomarker assessment, and CMR at 3.0T including assessment of left ventricular ejection fraction and LGE. Global longitudinal strain from two- and four-chamber cines was measured using feature tracking. Results: A total of 17/100 patients with no history of cardiovascular disease had silent MI defined by LGE in an infarct pattern on CMR. Only four patients with silent MI had Q waves on ECG. Patients with silent MI were older (65 vs 60, P = .05), had lower E/A ratio (0.75 vs 0.89, P = .004), lower GLS (–15.2% vs –17.7%, P = .004), and higher amino-terminal pro brain natriuretic peptide (106 ng/L vs 52 ng/L, P = .003). A combined risk score derived from these four factors had an area under the receiver operating characteristic curve of 0.823 (0.734–0.892), P < .0001. A score of more than 3/5 had 82% sensitivity and 72% specificity for silent MI. Conclusions: Using measures that can be derived in an outpatient clinic setting, we have developed a novel screening tool for the detection of silent MI in type 2 diabetes. The screening tool had significantly superior diagnostic accuracy than current ECG criteria for the detection of silent MI in asymptomatic patients.

Hypertensive Emergency and Type 2 Myocardial Infarction Resulting From Pheochromocytoma and Concurrent Capnocytophaga Canimorsus Infection

A diagnosis of myocardial infarction is made using a combination of clinical presentation, electrocardiogram and cardiac biomarkers. However, myocardial infarction can be caused by factors other than coronary artery plaque rupture and thrombosis. We describe an interesting case presenting with hypertensive emergency and type 2 myocardial infarction resulting from Pheochromocytoma associated with Capnocytophaga canimorsus infection from a dog bite. We also review current literature on the management of hypertensive emergency and Pheochromocytoma.

4 Four-dimensional left ventricular blood flow energetics independently predict adverse remodelling post st-elevation myocardial infarction

Introduction Myocardial infraction (MI) leads to complex changes in left ventricular (LV) haemodynamics. It remains unknown how four-dimensional (4D) acute changes in LV-cavity blood flow kinetic energy (KE) affect LV remodelling. We hypothesised that LV blood flow energetics is independently associated with adverse LV-remodelling. Methods We recruited 69 revascularised ST-elevation MI patients. All patients underwent cardiovascular magnetic resonance (CMR) at 1.5 T within 48 hours and at 3 months. CMR included cines, early/late gadolinium enhancement and whole-heart 4D flow. CMR analysis included: LV volumes, infarct size (IS,%), microvascular obstruction (MVO,%), two-dimensional, retrospective valve tracking derived mitral inflow metrics and 4D KE components. KE was derived using novel, semi-automated method by using endocardial contours on short-axis cines to extract intra-cavity velocity profile. Adverse LV-remodelling was defined as increase in LV end-diastolic volume by 15%. Results Thirteen (19%) patients developed adverse LV-remodelling. Demographics were comparable between patients with/without remodelling. Baseline CMR in adverse LV-remodelling-group showed significantly lower EF, LV KE, Systolic, A-wave, in-plane KEs and increased MVO (p<0.05). In stepwise-regression analysis, only acute MVO (beta=0.17±0.06, p<0.05) and acute A-wave KE (beta=−0.17±0.08, p<0.05) independently predicted adverse remodelling at 3 months. A regression-model comprising of acute MVO and A-wave KE had high predictive value for adverse LV-remodelling (area under the curve=0.82, 95% confidence interval=0.7–0.9, p<0.001). Conclusion LV haemodynamic assessment by novel, semi-automated, 4D KE mapping adds incremental value to predict adverse LV-remodelling. A-wave KE and MVO size early after acute MI are independently associated with adverse LV-remodelling.

Left ventricular thrombus formation in myocardial infarction is associated with altered left ventricular blood flow energetics

Abstract Aims The main aim of this study was to characterize changes in the left ventricular (LV) blood flow kinetic energy (KE) using four-dimensional (4D) flow cardiovascular magnetic resonance imaging (CMR) in patients with myocardial infarction (MI) with/without LV thrombus (LVT). Methods and results This is a prospective cohort study of 108 subjects [controls = 40, MI patients without LVT (LVT− = 36), and MI patients with LVT (LVT+ = 32)]. All underwent CMR including whole-heart 4D flow. LV blood flow KE wall calculated using the formula: KE=12 ρblood . Vvoxel . v2, where ρ = density, V = volume, v = velocity, and was indexed to LV end-diastolic volume. Patient with MI had significantly lower LV KE components than controls (P < 0.05). LVT+ and LVT− patients had comparable infarct size and apical regional wall motion score (P > 0.05). The relative drop in A-wave KE from mid-ventricle to apex and the proportion of in-plane KE were higher in patients with LVT+ compared with LVT− (87 ± 9% vs. 78 ± 14%, P = 0.02; 40 ± 5% vs. 36 ± 7%, P = 0.04, respectively). The time difference of peak E-wave KE demonstrated a significant rise between the two groups (LVT−: 38 ± 38 ms vs. LVT+: 62 ± 56 ms, P = 0.04). In logistic-regression, the relative drop in A-wave KE (beta = 11.5, P = 0.002) demonstrated the strongest association with LVT. Conclusion Patients with MI have reduced global LV flow KE. Additionally, MI patients with LVT have significantly reduced and delayed wash-in of the LV. The relative drop of distal intra-ventricular A-wave KE, which represents the distal late-diastolic wash-in of the LV, is most strongly associated with the presence of LVT.

New Cardiac Magnetic Resonance Reference Ranges for Right Ventricular Volumes and Systolic Function: What Is New and Why Should We Care?

Accurate quantitation of right ventricular (RV) volumes and systolic function provides important diagnostic and prognostic information in a wide range of conditions. In the case of heart failure, a preserved RV ejection fraction (RVEF) is associated with improved long-term survival.1 The most recent task force criteria for the diagnosis of arrhythmogenic RV cardiomyopathy require the presence of abnormal measurements of RV end-diastolic volume or RVEF to fulfil the major imaging criterion for diagnosis of the condition.2 In pulmonary arterial hypertension, increased RV end-diastolic volume and decreased RV stroke volume independently predict mortality3 and after myocardial infarction, RV function is an independent prognostic marker of clinical outcome.4 See Article by Foppa et al Cardiac magnetic resonance (CMR) is considered the current reference standard for quantitation of RV volumes and systolic function5 because of its accuracy and reproducibility, and several previous studies have reported normal values for this method. So why then do we need new normal reference values? CMR methods have undergone considerable evolution and standardization during the past 2 decades. Today, balanced steady-state free precession (SSFP) is the standard for acquisition of cine CMR images because it provides much better endocardial border delimitation, shorter scan times, and higher signal:noise ratios than the formerly used spoiled gradient echo methods.6 The overall better image quality of balanced SSFP acquisition and the ability to more clearly differentiate trabeculation …

Impact of Age and Diastolic Function on Novel, 4D flow CMR Biomarkers of Left Ventricular Blood Flow Kinetic Energy

Two-dimensional (2D) methods of assessing mitral inflow velocities are pre-load dependent, limiting their reliability for evaluating diastolic function. Left ventricular (LV) blood flow kinetic energy (KE) derived from four-dimensional flow cardiovascular magnetic resonance imaging (4D flow CMR) may offer improvements. It remains unclear whether 4D LV blood flow KE parameters are associated with physiological factors, such as age when compared to 2D mitral inflow velocities. Fifty-three healthy volunteers underwent standard CMR, plus 4D flow acquisition. LV blood flow KE parameters demonstrated good reproducibility with mean coefficient of variation of 6 ± 2% and an accuracy of 99% with a precision of 97%. The LV blood flow KEiEDV E/A ratio demonstrated good association to the 2D mitral inflow E/A ratio (r = 0.77, P < 0.01), with both decreasing progressively with advancing age (P < 0.01). Furthermore, peak E-wave KEiEDV and A-wave KEiEDV displayed a stronger association to age than the corresponding 2D metrics, peak E-wave and A-wave velocity (r = −0.51 vs −0.17 and r = 0.65 vs 0.46). Peak E-wave KEiEDV decreases whilst peak A-wave KEiEDV increases with advancing age. This study presents values for various LV blood flow KE parameters in health, as well as demonstrating that they show stronger and independent correlations to age than standard diastolic metrics.

49 Reduced myocardial perfusion reserve in systolic heart failure a therapeutic target

Background Left ventricular systolic dysfunction (LVSD) is associated with reduced myocardial perfusion reserve (MPR) even in the absence of proven ischaemic heart disease and patients may have typical angina symptoms, despite the lack of obstructive coronary artery disease. The severity of MPR reduction has been suggested as a prognostic marker in both ischaemic and non-ischaemic cardiomyopathy. We hypothesised that reduction in MPR was associated with worsening symptomatology (NYHA class) and systolic dysfunction (ejection fraction, EF). Methods 40 patients referred from cardiology clinics with LVSD of unknown cause underwent adenosine stress perfusion CMR (Siemens 3T). First pass stress and rest myocardial perfusion CMR data were acquired in three short axis slices with 0.05 mmol/kg intravenous Gadovist using a recently reported free-breathing motion corrected Method with in-line quantification of perfusion maps. For stress, adenosine was administered at 140 mcg/kg/min over 5 min. Segments showing regional perfusion defects or containing scar were excluded from further quantitative analysis. Myocardial blood flow (MBF) was calculated globally for the remaining left ventricle. Patients with no evidence of LVSD (EF-55%) were excluded from analysis. NYHA class was recorded at the time of CMR scan. EF was calculated from a short axis cine data set and classified as: mild (45%), moderate (3544%) and severe (34%) impairment. ANOVA with post hoc Bonferroni correction was used to compare means of the three groups. Results Patients were grouped both by NYHA class and by EF severity, comparisons of these groups are shown in Table 1. No significant difference was seen between groups with respect to age, resting heart rate and resting MBF. Abstract 49 Table 1 Comparison of patient groups NYHA I NYHA II NHYA III P N 15 12 7 Age 65.7±7.7 71.4±12.9 68.4±11.2 0.39 EF% 35.1±10.7 30.0±11.4 27.9±5.9 0.24 Resting HR 67.0±12.3 70.5±9.7 70.6±18.8 0.81 Rest MBF (ml/g/min) 0.67±0.28 0.77±0.34 0.67±0.30 0.68 Stress MBF (ml/g/min) 1.92±0.96 1.49±0.57 1.00±0.62 0.04 MPR 2.90±0.96 2.05±0.61 1.45±0.45 < 0.01 Mild Moderate Severe N 4 8 22 Age 60.4±7.12 71.1±6.36 68.7±11.7 0.242 Rest HR 67.5±10.6 61.8±8.52 72.2±13.6 0.139 Rest MBF(ml/g/min) 0.56±0.18 0.83±0.44 0.68±0.25 0.314 Stress MBF (ml/g/min) 1.78±0.658 1.89±1.06 1.43±0.76 0.379 MPR 3.21±0.86 2.38±0.91 2.11±0.91 0.093 *significant at level p=0.05, ** significant at level p=0.01 MPR was associated with NYHA class (figure 1). A greater reduction in MPR was associated with a higher NYHA class and there was a significant decrease in MPR between asymptomatic patients and those with exercise limitation (Mean MPR 2.90±0.96, 2.05±0.61, 1.45±0.45 for classes I, II and III respectively, p<0.01). No significant difference was seen between NYHA II and III (2.05 vs 1.45, p=0.32) although a trend to decreasing MPR was observed. Myocardial perfusion reserve did not correlate with severity of LV dysfunction (figure 2). Abstract 49 Figure 1 Abstract 49 Figure 2 Conclusion A reduction in MPR is associated with NYHA class in systolic heart failure, independent of ejection fraction. These findings suggest potential therapeutic targets for symptomatic improvement, including use of vasodilators, even in the absence of coronary disease.