Reference Myocardium Research Articles

Modeling of factors affecting late gadolinium enhancement kinetics in MRI of cardiac amyloid

BackgroundLate gadolinium enhancement (LGE) is a valuable part of cardiac magnetic resonance imaging (CMR). In particular, inversion-recovery imaging of LGE, with nulling of the signal from reference areas of myocardium, can have a distinctive pattern in some patients with cardiac amyloid, including both diffuse (relatively faint) subendocardial LGE and a relatively dark appearance of the blood. However, the underlying reasons for this distinctive appearance have not previously been well investigated. Pharmacokinetic modeling of myocardial contrast enhancement kinetics can potentially provide insight into the mechanisms of the distinctive LGE appearance that can be seen in cardiac amyloid, as well as why it may be unreliable in some patients. MethodsAn interactive three-compartment pharmacokinetic model of the dynamics of myocardial contrast enhancement in CMR was implemented, and used to simulate LGE dynamics in normal, scar, and cardiac amyloid myocardium; the results were compared with previously published values. ResultsThe three-compartment model is able to capture the qualitative features of LGE, in patients with cardiac amyloid. In particular, the characteristic “dark blood” appearance of PSIR images of LGE in cardiac amyloid is seen to likely primarily reflect expansion of the extravascular extracellular space (EES) by amyloid in the “reference” myocardium; the cardiac amyloid contrast enhancement dynamics also reflect expansion of the body EES. ConclusionThe distinctive appearance of LGE in cardiac amyloid is likely due to a combination of diffuse expansion by amyloid of the EES of the reference myocardium and of the body EES.

The peri-infarct gray zone of myocardial fibrosis is a better predictor of ventricular arrhythmias than dense core fibrosis in patients with previous myocardial infarction

Abstract Background Current sudden cardiac death (SCD) risk stratification relies heavily on left ventricular ejection fraction (LVEF), but markers to refine risk assessment are needed. Dense core fibrosis (DCF) and peri-infarct “gray zone” of myocardial fibrosis (GZF) on late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR) have been proposed as potential arrhythmogenic substrates. The aim of our study was to determine whether DCF and GZF could predict the occurrence of ventricular arrhythmias in patients with previous myocardial infarction. Methods We performed a single centre retrospective study enrolling consecutive patients with previous myocardial infarction undergoing CMR before implantable cardioverter-defibrillator (ICD) implantation. Areas of LGE were subdivided into “core” DCF and “peri-infarct” GZF zones based on signal intensity (>5 SD, and 2–5 SD above the mean of reference myocardium, respectively). The primary endpoint was a composite of sudden arrhythmic death, appropriate ICD shock, ventricular fibrillation (VF), or sustained ventricular tachycardia (VT) as detected by the device. Results A total of 88 patients (median age 61 years [IQR 54–73], 84% male, median LVEF 30% [IQR 23–36%], 14% secondary prevention) were included. During a median follow-up of 23 months [IQR 9–38], 13 patients reached the primary endpoint (10 appropriate ICD shock, 2 sustained VT or VF, and 1 sudden arrhythmic death). Patients who attained the primary endpoint had similar DCF (30.4±14.7 g vs. 28.0±15.3 g; P=0.601) but a greater amount of GZF (18.1±9.6 g vs. 11.9±6.7 g; P=0.005). On univariate analysis, GZF was associated with the composite endpoint (HR: 1.09 per gram; 95% CI: 1.02–1.15; P=0.006), whereas DCF was not (HR: 1.01 per gram; 95% CI: 0.98–1.05; P=0.571). After adjustment for LVEF, GZF remained independently associated with the primary endpoint (adjusted HR: 1.06 per gram; 95% CI: 1.01–1.12; P=0.035). Decision tree analysis identified 11.9g of GZF as the best cut-off to predict life-threatening arrhythmic events. The primary endpoint occurred in 11 out of the 35 patients (31.4%) with GZF ≥11.9 g, but in only 2 of the 53 patients (3.8%) with GZF <11.9 g – Figure 1. Conclusions The extent of peri-infarct GZF seems to be a better predictor of ventricular arrhythmias than DCF. This parameter may be useful to identify a subgroup of patients with previous myocardial infarction at increased risk of life-threatening arrhythmic events. Funding Acknowledgement Type of funding sources: None.

ENDOTHELIAL PROGENITOR CELLS ENGINEERED TO OVER-EXPRESS ENDOTHELIAL NO-SYNTHASE AND THEIR EFFECT ON ARRHYTHMIC SUBSTRATE AS ASSESSED BY GRAY ZONE ANALYSIS - A SUB-STUDY OF THE ENACT-AMI TRIAL

ENDOTHELIAL PROGENITOR CELLS ENGINEERED TO OVER-EXPRESS ENDOTHELIAL NO-SYNTHASE AND THEIR EFFECT ON ARRHYTHMIC SUBSTRATE AS ASSESSED BY GRAY ZONE ANALYSIS - A SUB-STUDY OF THE ENACT-AMI TRIAL

The peri-infarct gray zone of myocardial fibrosis is a better predictor of ventricular arrhythmias than dense core fibrosis in patients with previous myocardial infarction

Abstract Funding Acknowledgements Type of funding sources: None. Background Current sudden cardiac death (SCD) risk stratification relies heavily on left ventricular ejection fraction (LVEF), but markers to refine risk assessment are needed. Dense core fibrosis (DCF) and peri-infarct "gray zone" of myocardial fibrosis (GZF) on late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR) have been proposed as potential arrhythmogenic substrates. The aim of our study was to determine whether DCF and GZF could predict the occurrence of ventricular arrhythmias in patients with previous myocardial infarction. Methods We performed a single centre retrospective study enrolling consecutive patients with previous myocardial infarction undergoing CMR before implantable cardioverter-defibrillator (ICD) implantation. Areas of LGE were subdivided into "core" DCF and "peri-infarct" GZF zones based on signal intensity (>5 SD, and 2-5 SD above the mean of reference myocardium, respectively). The primary endpoint was a composite of sudden arrhythmic death, appropriate ICD shock, ventricular fibrillation (VF), or sustained ventricular tachycardia (VT) as detected by the device. Results A total of 88 patients (median age 61 years [IQR 54-73], 84% male, median LVEF 30% [IQR 23-36%], 14% secondary prevention) were included. During a median follow-up of 23 months [IQR 9-38], 13 patients reached the primary endpoint (10 appropriate ICD shock, 2 sustained VT or VF, and 1 sudden arrhythmic death). Patients who attained the primary endpoint had similar DCF (30.4g ± 14.7 vs. 28.0g ± 15.3; P = 0.601) but a greater amount of GZF (18.1g ± 9.6 vs. 11.9g ± 6.7; P = 0.005). On univariate analysis, GZF was associated with the composite endpoint (HR: 1.09 per gram; 95%CI: 1.02-1.15; P = 0.006), whereas DCF was not (HR: 1.01 per gram; 95%CI: 0.98-1.05; P = 0.571). After adjustment for LVEF, GZF remained independently associated with the primary endpoint (adjusted HR: 1.06 per gram; 95% CI: 1.01-1.12; P = 0.035). Decision tree analysis identified 11.9g of GZF as the best cut-off to predict life-threatening arrhythmic events. The primary endpoint occurred in 11 out of the 35 patients (31.4%) with GZF ≥11.9g, but in only 2 of the 53 patients (3.8%) with GZF <11.9g – Figure. Conclusions The extent of peri-infarct GZF seems to be a better predictor of ventricular arrhythmias than DCF. This parameter may be useful to identify a subgroup of patients with previous myocardial infarction at increased risk of life-threatening arrhythmic events.

PO-626-04 THE PERI-INFARCT “GRAY ZONE” OF MYOCARDIAL FIBROSIS IS A BETTER PREDICTOR OF VENTRICULAR ARRHYTHMIAS THAN DENSE CORE FIBROSIS IN PATIENTS WITH PREVIOUS MYOCARDIAL INFARCTION

Current sudden cardiac death (SCD) risk stratification relies heavily on left ventricular ejection fraction (LVEF), but markers to refine risk assessment are needed. Dense core fibrosis (DCF) and peri-infarct “gray zone” of myocardial fibrosis (GZF) on late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR) have been proposed as arrhythmogenic substrates. We aimed to determine whether DCF and GZF could predict the occurrence of ventricular arrhythmias in patients with previous myocardial infarction. We performed a single centre retrospective study enrolling consecutive patients with previous myocardial infarction undergoing CMR before implantable cardioverter-defibrillator (ICD) implantation. Areas of LGE were subdivided into “core” DCF and “peri-infarct” GZF zones based on signal intensity (>5 SD, and 2-5 SD above the mean of reference myocardium, respectively). The primary endpoint was a composite of sudden arrhythmic death, appropriate ICD shock, ventricular fibrillation (VF), or sustained ventricular tachycardia (VT) as detected by the device. A total of 88 patients (median age 61 years [IQR 54-73], 84% male, median LVEF 30% [IQR 23-36%]) were included. During a median follow-up of 23 months [IQR 9-38], 13 patients reached the primary endpoint. Patients who attained the primary endpoint had similar DCF (30.4g ± 14.7 vs. 28.0g ± 15.3; P = 0.601) but a greater amount of GZF (18.1g ± 9.6 vs. 11.9g ± 6.7; P = 0.005). On univariate analysis, GZF was associated with the composite endpoint (HR: 1.09 per gram; 95%CI: 1.02-1.15; P=0.006), whereas DCF was not (HR: 1.01 per gram; 95%CI: 0.98-1.05; P=0.571). After adjustment for LVEF, GZF remained independently associated with the primary endpoint (adjusted HR: 1.06 per gram; 95% CI: 1.01-1.12; P=0.035). Decision tree analysis identified 11.9g of GZF as the best cut-off to predict arrhythmic events. The primary endpoint occurred in 11 out of the 35 patients (31.4%) with GZF ≥11.9g, but in only 2 of the 53 patients (3.8%) with GZF <11.9g - Figure. The extent of peri-infarct GZF seems to be a better predictor of ventricular arrhythmias than DCF. This parameter may be useful to identify a subgroup of patients with previous myocardial infarction at increased risk of life-threatening arrhythmic events.

The gray zone of myocardial fibrosis is a better predictor of ventricular arrhythmias than total myocardial fibrosis in patients with previous myocardial infarction

Abstract Background Current sudden cardiac death (SCD) risk stratification relies heavily on the assessment of left ventricular ejection fraction (LVEF), but markers that could refine risk assessment are needed. Total fibrosis mass (TFM) and “gray zone” of myocardial fibrosis (GZF) on late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) have been proposed as potential arrhythmogenic substrates. The aim of our study was to determine whether TFM and GZF can predict the occurrence of ventricular arrhythmias in patients with previous myocardial infarction. Methods We performed a single centre retrospective study enrolling all consecutive patients with previous myocardial infarction undergoing LGE-CMR before implantable cardioverter-defibrillator (ICD) implantation for primary or secondary prevention. TFM and GZF were defined as myocardial tissue with signal-intensities &amp;gt;6 SD and 2–6 SD above the mean of reference myocardium, respectively. The primary endpoint was a composite of sudden arrhythmic death, appropriate ICD shock, ventricular fibrillation (VF), or sustained ventricular tachycardia (VT) as detected by the device. Results A total of 55 patients (mean age 62±12 years, 87% male, mean LVEF 30% ± 8%) were included. During a mean follow-up period of 34±15 months, 10 patients reached the primary endpoint (8 appropriate ICD shock, 2 sustained VT or VF). Patients who attained the primary endpoint had similar TFM (28.6g ± 14.5 vs. 23.1g ± 14.5; P=0.283) but larger GZF (25.3g ± 11.0 vs 15.6g ± 7.3; P=0.001). After adjustment for LVEF, GZF remained independently associated with the composite arrhythmic endpoint (adjusted hazard ratio [aHR]: 1.10; 95% CI: 1.03–1.17; P=0.005), whereas TFM did not (aHR: 1.02; 95% CI: 0.98–1.06; P=0.394). Decision tree analysis identified 16.4g of GZF as the best cut-off to predict life-threatening arrhythmic events. The primary endpoint occurred in 9 out of the 22 patients (41%) with GZF &amp;gt;16.4g, but in only 1 of the 33 patients (3%) with GZF ≤16.4g – Figure. Conclusions The extent of GZF seems to be a better predictor of ventricular arrhythmias than TFM. This LGE-CMR parameter may be useful to identify a subgroup of patients with previous myocardial infarction at an increased risk of life-threatening arrhythmic events. Funding Acknowledgement Type of funding sources: None.

Hinge point fibrosis is highly prevalent in male elite water polo players

Abstract Background/Introduction The grey zone between cardiac adaptation to sports and exercise and (early stages of) cardiac pathology constitutes one of the greatest challenges for clinicians involved in the care for (elite level) athletes. Cardiac magnetic resonance imaging (CMR) with late gadolinium enhancement (LGE) is a central diagnostic tool to help differentiate between physiological adaptation and pathology. LGE as seen in myocardial fibrosis has been shown to be a strong predictor for cardiac events. While general (ie. dynamic, static sports) levels of physiological adaptation in athletes have been described, sports-specific CMR findings are essentially lacking, and a systematic sport-specific investigation of LGE is absent. Purpose To establish a sports-specific baseline for CMR indices in apparently healthy, male elite water polo players. Methods We performed a cross-sectional study in Olympic-level male water polo players. All athletes were asymptomatic and were examined during pre-participation screening. The athletes underwent a comprehensive CMR protocol consisting of long- and short-axis cine imaging, LGE and was performed on two 3 Tesla MRI-scanners (Philips). CMR data were analysed using Circle Cardiovascular Imaging software, and statistical analyses were performed in R. Results We screened 24 athletes with a mean age (±SD) of 24.2±3.6 years and body surface area (BSA) of 2.23±0.2 m2. The athletes had indexed end-diastolic volumes of 101.87±33.01 ml and 104.51±43.24 ml, stroke volumes of 140.70±33.23 and 139.44±29.93 ml, and ejection fractions of 56.68±9.07% and 52.98±8.18%, in the left- and right ventricle, respectively. Thirteen athletes (54.2%) had LGE consistent with hinge point fibrosis (HPF+) (one case example presented in the figure). Another two athletes had other patterns of LGE (LGE+). There was a trend towards having a smaller BSA in the LGE+ and HPF+ groups (2.18±0.17 m2 in LGE+ vs 2.31±0.10 m2 in LGE−, p=0.056, and 2.18±0.18 m2 in HPF+ vs 2.29±0.10 m2 in HPF−, p=0.072). Conclusion Myocardial fibrosis is present in more than 50% of asymptomatic elite water polo players, with a predilection for the inferior hinge point. Our findings in asymptomatic elite athletes suggest that HPF could be a normal finding in athletes instead of an early sign of pathology. Further studies are warranted to investigate if the HPF is associated with long-term cardiac changes or the development of cardiac pathology. Figure 1. Late gadolinium enhanced short axis image (left) combined with a polar map of cardiac segmentation (right) depicting the fibrosis pattern in a case of an elite male water polo player alongside the inferior hinge point - as expressed in the percentage of myocardium exceeding the mean signal intensity of reference myocardium plus six-times standard deviation. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Harald Jørstad has received funding from the Amsterdam Movement Sciences and the National Olympic Committee &amp; National Sports Federation

Comparison of Magnetic Resonance Analysis of Myocardial Scarring With Biomarker Release Following S-T Elevation Myocardial Infarction

Late gadolinium enhancement (LGE) with cardiac magnetic resonance (CMR) is commonly assumed to represent myocardial fibrosis; however, comparative human histological data are limited, and there is no consensus on the most accurate method for LGE quantitation. We evaluated the relationship between CMR assessment of regional fibrosis and infarct size assessment using serial biomarkers after ST elevation acute myocardial infarction (STEMI). Ninety-three patients treated for STEMI (59±10 years, 86% male) underwent CMR 6 months after infarction. Infarct size was quantified by CMR-LGE using manual and range of semi-automated thresholds (range: 2-10 standard deviations [SD]) above reference myocardium and the full width-half maximum (FWHM) technique, and compared with the rise in serum biomarkers. The agreement between CMR and biomarker in the identification of large infarcts based on peak troponin (TnI) levels was also analysed. Quantification methods had a strong influence on the infarct size assessment with CMR-LGE. Significant correlations were observed between LGE and biomarkers across all of the signal intensity thresholds. Whilst there was a wide variation with respect to the estimation of total LGE size (from 6.8±7.7 to 32.1±11.3 grams), the variation in the correlation with peak troponin level was much smaller (r-values ranging from 0.670 to 0.876). There was good agreement between CMR-LGE and biomarker assessment of infarct size; the best agreement between CMR-LGE and large infarction using a threshold of 8SD for peak TnI>50ng/mL (Cohen's kappa (κ)=0.722), and a threshold of 4SD for peak TnI >95ng/mL (κ=0.761). The correlation between CMR-LGE quantification of infarct size and biomarker release following STEMI at a range of semi-automated thresholds was consistently strong, with good agreement between measures across a range of thresholds.

Effect of Ischemia Duration and Protective Interventions on the Temporal Dynamics of Tissue Composition After Myocardial Infarction.

The impact of cardioprotective strategies and ischemia duration on postischemia/reperfusion (I/R) myocardial tissue composition (edema, myocardium at risk, infarct size, salvage, intramyocardial hemorrhage, and microvascular obstruction) is not well understood. To study the effect of ischemia duration and protective interventions on the temporal dynamics of myocardial tissue composition in a translational animal model of I/R by the use of state-of-the-art imaging technology. Four 5-pig groups underwent different I/R protocols: 40-minute I/R (prolonged ischemia, controls), 20-minute I/R (short-duration ischemia), prolonged ischemia preceded by preconditioning, or prolonged ischemia followed by postconditioning. Serial cardiac magnetic resonance (CMR)-based tissue characterization was done in all pigs at baseline and at 120 minutes, day 1, day 4, and day 7 after I/R. Reference myocardium at risk was assessed by multidetector computed tomography during the index coronary occlusion. After the final CMR, hearts were excised and processed for water content quantification and histology. Five additional healthy pigs were euthanized after baseline CMR as reference. Edema formation followed a bimodal pattern in all 40-minute I/R pigs, regardless of cardioprotective strategy and the degree of intramyocardial hemorrhage or microvascular obstruction. The hyperacute edematous wave was ameliorated only in pigs showing cardioprotection (ie, those undergoing short-duration ischemia or preconditioning). In all groups, CMR-measured edema was barely detectable at 24 hours postreperfusion. The deferred healing-related edematous wave was blunted or absent in pigs undergoing preconditioning or short-duration ischemia, respectively. CMR-measured infarct size declined progressively after reperfusion in all groups. CMR-measured myocardial salvage, and the extent of intramyocardial hemorrhage and microvascular obstruction varied dramatically according to CMR timing, ischemia duration, and cardioprotective strategy. Cardioprotective therapies, duration of index ischemia, and the interplay between these greatly influence temporal dynamics and extent of tissue composition changes after I/R. Consequently, imaging techniques and protocols for assessing edema, myocardium at risk, infarct size, salvage, intramyocardial hemorrhage, and microvascular obstruction should be standardized accordingly.

Quantification of Infarct Size in Acute and Chronic Ischaemic and Non-Ischaemic Heart Diseases: Reproducibility of Different Techniques

Background: Several techniques have been proposed for the quantification of late gadolinium enhancement (LGE), including manual planimetry, manual thresholding, the signal threshold versus reference myocardium technique (STRM) and the full width at half maximum (FWHM) technique. However, none of these approaches is considered as the optimal method for quantitative assessment of left ventricular (LV) scar. This study compares the intra- and inter-observer reproducibility of the aforementioned quantification techniques across different disease processes that give rise to LV scar, i.e. acute myocardial infarct (AMI), acute myocarditis (AMy), chronic ischaemic heart disease (CIHD), hypertrophic cardiomyopathy (HCM) and non-ischaemic cardiomyopathy (NICM). Methods: 100 patients (20 AMI patients, 20 AMy patients, 20 CIHD patients, 20 HCM patients and 20 NICM patients) who had cardiac magnetic resonance imaging and visually detectable LGE were included in the study. LGE images were analysed by two independent observers and intra- and inter-observer agreement of each technique was reported using the intraclass correlation coefficient (ICC). Results: All quantitative techniques had excellent intra- and inter-observer agreement (ICC values ≥0.95) in AMI patients, while only FWHM performed well in AMy and CIHD patients (intra- and inter-observer ICC were 0.96 and 0.92 among AMy patients and 0.95 and 0.93 among the CIHD patients). Among HCM and NICM patients, all quantitative techniques had good intra- and inter-observer agreement (ICC values ≥0.90), except manual thresholding, which had ICC values <0.90; FWHM presented the highest intra- and inter-observer ICC (0.97 and 0.94, respectively). Conclusions: FWHM technique performs well in all cardiac conditions; STRM techniques represent a valid alternative in AMI, HCM and NICM.

Temporal change of myocardial tissue character is associated with left ventricular reverse remodeling in patients with dilated cardiomyopathy: A cardiovascular magnetic resonance study

BackgroundPrognostic significance of temporal change in myocardial tissue characterization by cardiovascular magnetic resonance (CMR) has not been elucidated in patients with non-ischemic dilated cardiomyopathy (DCM). Methods and resultsSixty-eight patients with newly-diagnosed DCM who underwent CMR including late gadolinium enhancement (LGE) both at baseline and during follow-up period were enrolled. LGE score was defined by a signal intensity of ≥5 standard deviations above the remote reference myocardium mean. Left ventricular reverse remodeling (LVRR) defined as a LV ejection fraction increase of ≥10% and a decrease in indexed LV end-diastolic diameter of ≥10% compared to those at baseline was detected in 38% of the patients. There was no significant difference in LGE score between baseline and follow-up (5.8% vs. 7.3%; p=0.38). The change in LGE area (delta-LGE) was significantly lower in patients with LVRR than those without (−0.5%±3.4% vs. 3.0±7.4%; p=0.02). On the other hand, T2 ratio during the follow-up significantly reduced (1.95±0.48 vs. 1.67±0.56; p<0.01); however, there was no significant difference in the change in T2 ratio between patients with LVRR and those without (−0.29±0.73 vs. −0.27±0.66; p=0.88). Multivariate logistic analysis indicated that baseline LGE score [odds ratio; 0.78; 95% confidence interval (CI) 0.66 to 0.90; p<0.01] together with delta-LGE (odds ratio; 0.77; 95% CI 0.61 to 0.92; p=0.01) were independently associated with subsequent LVRR (p<0.01). ConclusionsThe temporal change of LGE-CMR score during the clinical course was significantly correlated with following LVRR.

Measurement of myocardial native T1 in cardiovascular diseases and norm in 1291 subjects

BackgroundNative T1-mapping provides quantitative myocardial tissue characterization for cardiovascular diseases (CVD), without the need for gadolinium. However, its translation into clinical practice is hindered by differences between techniques and the lack of established reference values. We provide typical myocardial T1-ranges for 18 commonly encountered CVDs using a single T1-mapping technique – Shortened Look-Locker Inversion Recovery (ShMOLLI), also used in the large UK Biobank and Hypertrophic Cardiomyopathy Registry study.MethodsWe analyzed 1291 subjects who underwent CMR (1.5-Tesla, MAGNETOM-Avanto, Siemens Healthcare, Erlangen, Germany) between 2009 and 2016, who had a single CVD diagnosis, with mid-ventricular T1-map assessment. A region of interest (ROI) was placed on native T1-maps in the “most-affected myocardium”, characterized by the presence of late gadolinium enhancement (LGE), or regional wall motion abnormalities (RWMA) on cines. Another ROI was placed in the “reference myocardium” as far as possible from LGE/RWMA, and in the septum if no focal abnormality was present. To further define normality, we included native T1 of healthy subjects from an existing dataset after sub-endocardial pixel-erosions.ResultsNative T1 of patients with normal CMR (938 ± 21 ms) was similar compared to healthy subjects (941 ± 23 ms). Across all patient groups (57 ± 19 yrs., 65% males), focally affected myocardium had significantly different T1 value compared to reference myocardium (all p < 0.001). In the affected myocardium, cardiac amyloidosis (1119 ± 61 ms) had the highest native T1 compared to normal and all other CVDs, while iron-overload (795 ± 58 ms) and Anderson-Fabry disease (863 ± 23 ms) had the lowest native reference T1 (all p < 0.001). Future studies designed to detect the large T1 differences between affected and reference myocardium are estimated to require small sample-sizes (n < 50). However, studies designed to detect the small T1 differences between reference myocardium in CVDs and healthy controls can require several thousand of subjects.ConclusionsWe provide typical T1-ranges for common clinical cardiac conditions in the largest cohort to-date, using ShMOLLI T1-mapping at 1.5 T. Sample-size calculations from this study may be useful for the design of future studies and trials that use T1-mapping as an endpoint.

Late gadolinium enhancement does occur in Tako-tsubo cardiomyopathy — A quantitative cardiac magnetic resonance and speckle tracking strain study

BackgroundLate gadolinium enhancement (LGE) on cardiac magnetic resonance imaging (CMR) has been recommended to distinguish Tako-tsubo cardiomyopathy (TTC) from either acute myocardial infarction or myocarditis. Method44 consecutive patients with confirmed Mayo Clinic criteria for TTC underwent CMR imaging at 1.5Tesla during the acute phase. 10 patients who had CMRI to exclude scar related ventricular tachycardia, and had negative studies, were used as negative controls. LGE was quantitated at two signal intensity thresholds (CircleCVi software) at >2 and >5 standard-deviations (SD) above reference myocardium, and compared to biomarkers. FindingsMean door-to-CMR time was 57hours. 18 patients (41%) had LGE >2 SD localized to the area of abnormal wall motion, representing 28.9±11.2% LV mass. In 16 of these 18 patients (89%) LGE signal intensity was >5 SD above normal myocardium, representing 12.1±10% LV mass. LGE signal intensity was significantly greater in TTC than in matched controls (p<0.05) but lower than in STEMI patients (p<0.05). Mean troponin was significantly higher in LGE positive patients (2.5±1.8 vs 4.4±6.9, p=0.001). Mean ejection fraction (EF) by CMR was 45%±8.7 in LGE-negative, and 40%±7.1 in LGE-positive patients (p=0.37). Recovery of segmental function was confirmed at follow-up, mean EF was 59% in both groups. ConclusionLGE was present in 41% of cases of TTC, 89% of which had intense enhancement >5 SD above normal myocardium. Presence of LGE was associated with worse myocardial injury in the acute setting, with no difference in recovery of function.

Distribution and Clinical Significance of High Signal Intensity of the Myocardium on T2-Weighted Images in 2 Phenotypes of Hypertrophic Cardiomyopathy.

The aim of this study was to evaluate distribution and clinical significance of high signal intensity of the myocardium on T2-weighted images (T2-HI) in 2 phenotypes of hypertrophic cardiomyopathy (HCM). Thirty-six patients with asymmetrical septal HCM (ASH) and 18 patients with apical HCM (APH) and their 864 myocardial segments were investigated. The distribution of T2-HI was compared with that of late gadolinium enhancement (LGE), and the relationships between T2-HI and clinical risk markers were evaluated. T2 values of the T2-HI were estimated with T2 mapping. The T2-HI was observed in 18 segments (3.1%) in 13 patients with ASH (36.1%) and in 12 segments (4.2%) in 8 patients with APH (44.4%). It was often localized outside LGE. The presence of T2-HI was related to syncope in ASH (P = 0.016). Furthermore, it had higher T2 values (61.1 milliseconds) than the reference myocardium (47.3 milliseconds). High signal intensity of the myocardium on T2-weighted images often locates outside LGE and reflects myocardial damage, which is related to syncope in ASH.

Feasibility of dynamic CT-based adenosine stress myocardial perfusion imaging to detect and differentiate ischemic and infarcted myocardium in an large experimental porcine animal model

The purpose of the study is feasibility of dynamic CT perfusion imaging to detect and differentiate ischemic and infarcted myocardium in a large porcine model. 12 Country pigs completed either implantation of a 75% luminal coronary stenosis in the left anterior descending coronary artery simulating ischemia or balloon-occlusion inducing infarction. Dynamic CT-perfusion imaging (100kV, 300mAs), fluorescent microspheres, and histopathology were performed in all models. CT based myocardial blood flow (MBFCT), blood volume (MBVCT) and transit constant (Ktrans), as well as microsphere's based myocardial blood flow (MBFMic) were derived for each myocardial segment. According to histopathology or microsphere measurements, 20 myocardial segments were classified as infarcted and 23 were ischemic (12 and 14%, respectively). Across all perfusion states, MBFCT strongly predicted MBFMic (β 0.88±0.12, p<0.0001). MBFCT, MBVCT, and Ktrans were significantly lower in ischemic/infarcted when compared to reference myocardium (all p<0.01). Relative differences of all CT parameters between affected and non-affected myocardium were higher for infarcted when compared to ischemic segments under rest (48.4 vs. 22.6% and 46.1 vs. 22.9% for MBFCT, MBVCT, respectively). Under stress, MBFCT was significantly lower in infarcted than in ischemic myocardium (67.8±26 vs. 88.2±22ml/100ml/min, p=0.002). In a large animal model, CT-derived parameters of myocardial perfusion may enable detection and differentiation of ischemic and infarcted myocardium.

Going with the flow: how reproducible are cardiac magnetic resonance measurements of myocardial perfusion?

Myocardial perfusion imaging using cardiac magnetic resonance (CMR) is becoming a widely used clinical tool. With the recent publication of large scale clinical trials providing evidence for its high diagnostic accuracy in coronary heart disease, there is a growing evidential basis for CMR based perfusion measurements as an alternative to the most commonly used method, Single Photon Emission Computer Tomography (1,2). Clinically, CMR perfusion images are usually interpreted visually. This however introduces subjectivity to the analysis and so quantitative and semi-quantitative measurements have been devised to allow more objective assessments of myocardial blood flow. Such measurements may prove to be important for diagnosing coronary heart disease, especially in the case of multiple vessel disease, where the lack of healthy reference myocardium can render visual assessment unreliable.

Predictors of response to cardiac resynchronization therapy on pre-implantation cardiovascular magnetic resonance imaging

Background Cardiac resynchronization therapy (CRT) is an established treatment for severe heart failure. However, up to 40% of patients do not respond. While regional scar distribution has received focused attention, the predictive utility of global markers of remodeling and irreversible injury has not been well explored. Methods Sixty-eight patients receiving CRT underwent pre-implant cardiovascular MRI followed by serial echocardiography at 3 and 6 months. Blinded measurement of Left Ventricular (LV) and Right Ventricular (RV) chamber dimensions, volumes and mass were performed from short axis cine datasets. LV dysynchrony was measured by septal to lateral wall delay. Total LV scar burden was determined from Late Gadolinium Enhancement (LGE) images using manual contour tracing of endocardial and epicardial borders with application of a signal threshold ≥5SD above reference myocardium. Response to CRT was defined as a reduction in LV end-systolic volume (ESV) ≥15% at 6 months. Results The mean age was 66.3 ± 8.9 years with a mean LV Ejection fraction (EF) of 25.2 ± 7.2%. Overall, 47 patients (69%) responded. Among all baseline measures LVEDV (p=0.03), LVESV (p=0.045), RV EF (p=0.0349) and total scar burden (p=0.018) were the only significant predictors of CRT response. Multivariate analysis showed total scar burden to be the only independent predictor of CRT response (p=0.015). Conclusions Pre-implantation MRI offers markers for the prediction of response to CRT. Of these, total scar burden appears to be an independent predictor of response and may be of assistance in the selection of optimal candidates. Funding None

Quantitation of Late Gadolinium Enhancement in Tako-Tsubo Cardiomyopathy—A Cardiac Magnetic Resonance Study

Background: Late gadolinium enhancement (LGE) on cardiac magnetic resonance imaging (CMR) has been recommended to distinguish Tako-Tsubo cardiomyopathy (TTC) from either acute myocardial infarction or myocarditis. Method: Forty-four consecutive patients with confirmed Mayo Clinic criteria for TTC underwent CMR imaging at 1.5 Tesla during the acute phase. LGE was quantitated at two signal thresholds (CircleCVi software) at >2 and >5 standard-deviations (SD)above reference myocardium, and compared to biomarkers. Findings: Mean door-to-CMR time was 57 h. Eighteen patients (41%) had LGE >2SD localised to the area of abnormal wall motion, representing 28.9 ± 11.2% LV mass. In 16 of these 18 patients (89%) LGE was >5 SD above normal myocardium, representing 12.1 ± 10% LV mass. Mean troponin was significantly higher in LGE positive patients (2.5 ± 1.8 vs 4.4 ± 6.9, p = 0.001). Mean ejection fraction (EF) by CMR was 45 ± 8.7% in LGE-negative, and 40 ± 7.1 in LGE-positive patients (p = 0.37). Recovery of segmental function was confirmed at follow-up, mean EF was 59% in both groups. Conclusion: LGE was present in 41% of cases of TTC, 89% of which had intense enhancement >5 SD above normal myocardium. Presence of LGE was associated with worse myocardial injury in the acute setting, with no difference in recovery of function.

Comparison of scar signal quantification using phase corrected and conventional magnitude inversion recovery delayed enhancement imaging in patients with ischemic and non-ischemic cardiomyopathy

Background Myocardial scar volume quantification has been shown to predict response to medical, surgical, and device therapy. Phase sensitive inversion recovery (PSIR)-based Late Gadolinium Enhancement (LGE) image reconstruction is clinically attractive for its reduced dependence on accurate prescription of the Time from Inversion (TI time), and is becoming a preferred approach for many centers. However, while an efficient approach for the visual interpretation of myocardial injury, the influence of this approach on signal-threshold based scar volume quantification has been poorly explored. Methods A total of 80 patients with obvious myocardial scar by LGE imaging (40 ischemic, 40 non-ischemic) underwent blinded evaluations of total scar volume (%LV mass) using matched MIR and PSIR short axis images. Analysis was performed using the Signal Threshold Versus Reference Myocardium (STRM) technique at ≥2, ≥3, and ≥5 SD thresholds. In those with ischemic scar the Full Width at Half Maximum (FWHM) approach was incrementally evaluated. Linear regression and BlandAltman analyses comparing MIR verses PSIR-based scar quantification was performed. Results Linear regression analysis demonstrated an excellent correlation between PSIR and MIR-based STRM scar volumes at all 3 STRM-based thresholds for both ischemic scar (r=0.96, 0.95, and 0.88, respectively) and non-ischemic scar (r=0.86, 0.89, 0.90, respectively). FWHM analysis showed good correlation in ischemic scar (r=0.83). Bland-Altman analysis of STRM analysis showed a systematic bias with lower scar volumes produced by PSIR reconstruction images for both ischemic and non-ischemic scar. These differences were modest using STRM for ischemic scar (-3.3, -4.0 and -4.9%,

Longitudinal rotating frame relaxation time measurements in infarcted mouse myocardium in vivo

Longitudinal relaxation time in the rotating frame (T1ρ) was measured using continuous wave irradiation in normal and infarcted mouse myocardium in vivo. Significant increase in T1ρ was found after 7 days of infarction when compared with reference myocardium or in myocardium before infarction. Cine MRI and histology were performed to verify the severity of infarction. The time course of T1ρ in the infarct fits better with granulation and scar tissue formation than necrosis and edema. The results of the study show that T1ρ could potentially be a noninvasive quantitative marker for tissue remodeling after ischemic damage.