Signal Intensity In Myocardium Research Articles

Cardiac magnetic resonance imaging detection of intramyocardial hemorrhage in patients with ST-elevated myocardial infarction: comparison between susceptibility-weighted imaging and T1/T2 mapping techniques.

Susceptibility-weighted imaging (SWI) and T1/T2 mapping can be used to detect reperfusion intramyocardial hemorrhage (IMH) in ST-segment elevation myocardial infarction (STEMI) patients. However, the sensitivity and accuracy of the SWI and T1/T2 mapping sequences were not systematically compared. The study aimed to evaluate image quality and diagnostic performance of SWI in patients with IMH, compared with T1/T2 mapping. A prospective study was conducted on consecutive acute STEMI patients who were recruited from January to July 2022. Within 2-6 days after reperfusion treatment, all patients underwent a 3T cardiac magnetic resonance (CMR) examination, including T2-weighted short-tau inversion recovery (T2W-STIR), T1/T2 mapping, and SWI. A total of 36 patients [age, 56.50±17.25 years; males, 83.33% (30/36)] were enrolled. The relative infarct-remote myocardium signal intensity ratio (SIinfarct-remote) and contrast-to-noise ratio (CNR) were calculated for each patient on T1/T2 mapping and SWI, and the difference between relative signal intensity-to-noise ratio (rSNR) in the IMH (rSNRIMH) was measured for IMH patients on T1/T2 mapping and SWI. SIinfarct-remote, CNR, and rSNRIMH were compared among the three sequences. Receiver operating characteristic (ROC) analyses were used to evaluate the diagnostic performance of three sequences by SIinfarct-remote and visual assessment. A total of 26 (72.22%) patients had IMH. Quantitatively, the SIinfarct-remote of three sequences had excellent diagnostic performance for detecting IMH [SWI area under the curve (AUC) =1.000, 95% confidence interval (CI): 1.000-1.000 vs. T1 mapping AUC =0.954, 95% CI: 0.885-1.000 vs. T2 mapping AUC =0.985, 95% CI: 0.955-1.000; SWI vs. T1 mapping, P=0.300; SWI vs. T2 mapping, P=0.188; T1 mapping vs. T2 mapping, P=0.302). Qualitatively, three sequences had similar performance on detecting IMH (SWI AUC =0.895, 95% CI: 0.784-1.000; T1 mapping AUC =0.835, 95% CI: 0.711-0.958; and T2 mapping AUC =0.855, 95% CI: 0.735-0.974; SWI vs. T1 mapping, P=0.172; SWI vs. T2 mapping, P=0.317; T1 mapping vs. T2 mapping, P=0.710). The rSNRIMH was highest in T1 mapping, followed by T2 mapping and SWI, but SWI had the highest CNR. SWI, as well as T1/T2 mapping, is a feasible and accurate approach for clinical diagnosis of IMH with excellent performance.

Patients with Post-COVID-19 Vaccination Myocarditis Have More Favorable Strain in Cardiac Magnetic Resonance Than Those With Viral Myocarditis.

There have been reports of myocarditis following vaccination against COVID-19. We sought to describe cardiac magnetic resonance (CMR) findings among pediatric patients. Retrospective review at a large academic center of patients clinically diagnosed with post-vaccine myocarditis (PVM) undergoing CMR. Data collected included parametric mapping, ventricular function, and degree of late gadolinium enhancement (LGE). Post-processing strain analysis was performed using feature tracking. Strain values, T1/T2 values, and ventricular function were compared to age- and gender-matched controls with viral myocarditis using a Wilcoxon Signed Rank test. Among 12 patients with presumed PVM, 11 were male and 11 presented after the second vaccination dose, typically within 4days. All presented with chest pain and elevated troponin. 10 met MRI criteria for acute myocarditis. All had LGE typically seen in the lateral and inferior walls; only five had prolonged T1 values. 10 met criteria for edema based on skeletal muscle to myocardium signal intensity ratio and only 5 had prolonged T2 mapping values. Patients with PVM had greater short-axis global circumferential and radial strain, right ventricle function, and cardiac output when compared to those with viral myocarditis. Patients with PVM have greater short-axis global circumferential and radial strains compared to those with viral myocarditis. LGE was universal in our cohort. Signal intensity ratios between skeletal muscle and myocardium may be more sensitive in identifying edema than T2 mapping. Overall, the impact on myocardial strain by CMR is less significant in PVM compared to more classic viral myocarditis.

Impact of coronary plaque characteristics on periprocedural myocardial injury after elective percutaneous coronary intervention -MDCT and CMR analysis-

Abstract Background Percutaneous coronary intervention (PCI) is often complicated by periprocedural myocardial injury (PMI) manifested by elevated cardiac biomarkers. The occurrence of PMI has been shown to be associated with worse clinical outcome over short- and long-term. Purpose We performed multidetector computed tomography (MDCT) and cardiac magnetic resonance imaging (CMR) to evaluate the relationship between culprit plaque characteristics and PMI. Methods A total of 90 patients who underwent elective PCI were underwent CMR and multidetector coronary tomography before PCI. The high intensity plaque (HIP) on CMR was defined as a coronary plaque to myocardium signal intensity ratio (PMR) of >1.4. The plaque characteristics and the presence of napkin-ring sign (NRS) were analyzed on MDCT. PMI was defined as an increase in cardiac Troponin T levels to more than 5 times the upper limit of normal at 24 h after PCI. Patients were divided into 2 groups according to the presence (Group I, n=26) or absence (Group II, n=64) of PMI. Results Spotty calcification, positive remodeling, low attenuation plaque and NRS on MDCT were significantly more observed in Group I than in Group II. HIP on CMR was significantly more observed in Group I than in Group II. In the multivariable logistic regression analysis, the presence of NRS and HIP were significantly independent predictors of PMI (odds ratio (OR) 4.82, 95% confidence interval 1.13–20.60, P=0.034 and OR 3.66, 95% CI 1.09–12.30, P=0.036, respectively). Moreover, for prediction of PMI, NRS and HIP showed a high positive predictive value of 81%, and their absence showed a high negative predictive value of 91%. Conclusions MDCT and CMR may play an important role in detecting which lesions are high risks for myocardial necrosis after PCI in elective coronary stenting. Funding Acknowledgement Type of funding source: None

158 Quantifying manganese-calcium interaction for optimal cardiac manganese enhanced mri

IntroductionInformation on myocardial viability is important for the management of ischaemic cardiomyopathy patient. Difficulties in assessing viability arise because necrotic tissue and viable myocardium overlap at the infarct border zone....

Coronary high-intensity plaque on T1-weighted magnetic resonance imaging and its association with myocardial injury after percutaneous coronary intervention.

Non-contrast T1-weighted imaging (T1WI) has emerged as a novel non-invasive imaging for vulnerable coronary plaque showing a high-intensity plaque (HIP). However, the association between HIP and percutaneous coronary intervention (PCI) has not been evaluated. We investigated the association between the presence of HIP and the incidence of myocardial injury after PCI. A total of 77 patients with stable angina were imaged with non-contrast T1WI by using a 1.5 T magnetic resonance system (HIP and non-HIP group, N = 31 and 46 patients, respectively). We defined HIP as a coronary plaque to myocardium signal intensity ratio (PMR) of ≥1.4. High-sensitive cardiac troponin-T (hs-cTnT) was measured at baseline and 24 h after PCI. Percutaneous coronary intervention-related myocardial injury (PMI) was defined as an elevation of hs-cTnT >5× 99th percentile upper reference limit. High-intensity plaque was associated with the characteristics of ultrasound attenuation and positive remodelling on intravascular ultrasound. Although baseline hs-cTnT was similar between the groups, increase in hs-cTnT was significantly greater in the HIP vs. non-HIP group (0.065 [0.023-0.304] vs. 0.017 [0.005-0.026], P < 0.001). Percutaneous coronary intervention-related myocardial injury occurred more frequently in the HIP than non-HIP group (58.1 vs. 10.9%, P < 0.001), and the cut-off value of PMR found to be 1.44 for predicting PMI (sensitivity 78.3% and specificity 81.5%). In multivariate analysis, a PMR of ≥1.4 was a significant predictor of PMI (odds ratio 5.63, 95% confidence interval 1.28-24.7, P = 0.022). High-intensity plaque on non-contrast T1WI was characterized as vulnerable coronary plaque on IVUS and was associated with higher incidence of PMI.

The comparison of MR intragate and electrocardiogram-respiration triggered fast low-angle shot in imaging the structure and function of the heart

Objective A comparison between intragate and ECG-respiration triggered techniques was performed to determine their differences in measuring the structure and function of the heart at 7.0 T.Methods Ten normal ICR mice aged five to six weeks were examined on a 7.0 T MR scanner.A central slice with papillary muscle included at the short-axis view was scanned with a FLASH-cine bright blood sequence,FLASH-cine black blood sequence,IG-FLASH-sat-cine black blood sequence,and IG-FLASH-cine bright blood sequence.The area of the left ventricle of the end systole and end diastole ( including and excluding the myocardium) was measured with manually outlined ROIs.The increased area of the left ventricle and the myocardium from the end systolic to end diastolic phases was calculated.The signal intensity was measured from 8 ROIs which were evenly located at the myocardium of the end systole,and the mean and standard deviation were then determined.The coefficient of variation ( CV ) was derived by dividing the mean into the standard deviation.Results There was no significant difference ( the increased area of the myocardium t =0,P =1,the increased area of the left ventricle t =2.12,P =0.06) in the function index between the ECG-triggered black blood sequences [the increased area of the myocardium (0.100 ±0.018) cm2,the increased area of the left ventricle (0.060 ± 0.024) cm2] and intragate black blood sequences[the increased area of the myocardium (0.090 ± 0.014) cm2,the increased area of the left ventricle (0.060 ±0.012) cm2].No significant difference(the increased area of the myocardium t =1.56,P =0.15,the increased area of the left ventricle t =2.08,P =0.07 ) in the function index was observed between the ECG-triggered bright blood sequences [the increased area of the myocardium ( 0.100 ±0.018) cm2,the increased area of the left ventricle(0.060 ±0.014) cm2]and intragate bright blood sequences [the increased area of the myocardium (0.090 ±0.019) cm2,the increased area of the left ventricle (0.050 ±0.015) cm2].Furthermore,there was no significant difference(t =1,P =0.34) in the CV of the myocardium signal intensity of bright blood sequences between the ECG-triggering ( 0.050 ± 0.013 ) and intragate (0.040 ± 0.015 ),but significant difference ( t =4.51,P =0.001 ) in the CV of the myocardium signal intensity of black blood sequences between the ECG-triggering ( 0.070 ± 0.033 ) and intragate ( 0.160 ± 0.046 ) was obtained.Conclusions The intragate sequences could take the place of the ECG gate sequences in functional analysis of the heart( including bright blood and black blood sequences).The bright blood intragate sequences also could replace the bright blood ECG-triggered sequences in analyzing the signal of the myocardium. Key words: Heart; Magnetic resonance imaging; Animal experimentation

Quantification of acute myocardial injury by ShMOLLI T1-Mapping, T2-weighted and late gadolinium imaging in patients presenting with chest pain, positive troponins and non-obstructive coronary arteries

Methods 16 patients (8 men, mean age 51±16 years) with acute chest pain, Troponin I >1.0 ug/L and non-obstructive coronary arteries underwent 1.5T CMR imaging within 7 days of presentation (median 3 days). CMR protocol included Shortened Modified Look-Locker inversion recovery (ShMOLLI) for T1-mapping, T2-STIR and late gadolinium enhancement (LGE) imaging. Regional wall motion was assessed with SSFP cines. Volumetric fractions of injured myocardium were quantified by (1) T2 signal intensity (SI) of myocardium:skeletal muscle >1.9:1; (2) T1>110% of normal myocardial T1; and (3) LGE SI>2SD of remote myocardium SI. Results 8 cases of myocarditis, 4 cases of Takotsubo cardiomyopathy and 4 cases of myocardial infarction were diagnosed based on CMR findings. All demonstrated abnormalities by at least 2 out of the 3 sequences (Table1). All but one (focal myocarditis) demonstrated global/focal increase in T2 SI. All demonstrated global/ focal increase in T1 values. Except for patients with Takotsubo cardiomyopathy, all demonstrated LGE. Volumetric fractions of injury by T2-STIR and T1mapping overlapped but did not necessarily co-localize topographically; there was moderate correlation between the two methods (R=0.45) (Fig.1). Patients with Takotsubo cardiomyopathy (mean EF=54 ±7%) had the highest average T1 values (1028±34ms vs. 968±76ms in normal controls; p<0.025*). Except for one with global myocarditis, patients with myocarditis and MI were without significant LVEF impairment with focal injury. Accordingly, average T1 values in these subgroups were not statistically different from normal. On a regional level, compared to segments with normal wall motion, segments with abnormal wall motion had significantly increased T1 values (958±60 ms vs.1068±76 ms, respectively; p<0.001*) (Fig.2), larger fractions of injury by T1-mapping (median 12% vs. 62%; p<0.001*), T2-STIR (15% vs. 62%; p<0.001*) and LGE (8% vs 10%; p<0.04*). LVEF correlated best with T1-mapping derived fractions of injured myocardium (R=0.59; T2-STIR R=0.18, LGE R=0.1). University of Oxford, Oxford, UK Full list of author information is available at the end of the article Ferreira et al. Journal of Cardiovascular Magnetic Resonance 2011, 13(Suppl 1):P16 http://jcmr-online.com/content/13/S1/P16

Real-Time Myocardial Contrast Echocardiography in Rat: Infusion Versus Bolus Administration

To compare the feasibility of real-time myocardial contrast echocardiography (MCE) in rats with infusion and bolus administration of a second-generation ultrasound contrast agent BR1. B-mode real-time MCE was performed in 12 Sprague Dawley rats following the BR1 infusion or bolus injection. The myocardium signal intensity (SI) was plotted against time and was fitted to exponential functions. The plateau SI (A) and rate of SI increase (β) for the infusion study and peak signal intensity (PSI) for the bolus study were obtained. 99mTc-Sestamibi and Evans blue were used to assess myocardial blood perfusion and to calculate the myocardium perfusion defect area ex vivo. High-quality real-time MCE images were successfully obtained using each method. At baseline, all LV segments showed even contrast distribution. Following left anterior descending coronary artery (LAD) ligation, significant perfusion defect was observed in LAD beds with a significantly decreased A* β and PSI values compared with LCx beds (Infusion: A*β LAD: 5.42 ± 1.57dB, A*β LCx: 46.52 ± 5.32dB, p < 0.05; Bolus: PSI LAD: 2.11 ± 0.67dB, PSI LCx: 20.68 ± 0.72 dB, p < 0.05), which was consistent with 99mTc-Sestamibi distribution findings. Myocardial perfusion defect areas, assessed by both methods, showed no differences and showed good correlation with Evans blue staining. ED frames were more favorable for imaging analysis. Both infusion and bolus administration of the contrast agent combined with real-time MCE technique can provide a reliable and noninvasive approach for myocardial perfusion assessment in rats and the infusion method was more suitable for quantitative analysis of myocardial blood flow. (E-mail: suhaili@fmmu.edu.cn)

Abstract P35: Real-time Myocardial Contrast Echocardiography in Rat: Infusion vs. Bolus Administration

AIM: To compare the feasibility of real-time myocardial contrast echocardiography (RTMCE) in rats with infusion and bolus administration of BR1. Methods: RTMCE was performed in 12 Sprague-Dawley rats using B-mode RTMCE following the BR1 infusion or bolus injection. The myocardium signal intensity (SI) was plotted against time and was fitted to exponential functions. The plateau SI (A) and rate of SI increase (â) for the infusion study and peak signal intensity (PSI) for the bolus study were obtained. 99m Tc-Sestamibi and Evans blue were used to assess myocardial blood perfusion and to calculate the myocardium perfusion defect area ex vivo . Results: High-quality RTMCE images were successfully obtained using each method. At baseline, all LV segments showed even contrast distribution (Figure A ). Following left anterior descending (LAD) aorta ligation, significant perfusion defect was observed in LAD beds (Figure B , arrows) with a significantly decreased A*â and PSI values compared to LCx beds (Infusion: A* â LAD : 5.42 ± 1.57dB, A* â LCx : 46.52 ± 5.32dB, p± 0.05; Bolus: PSI LAD : 2.11 ± 0.67dB, PSI LCx : 20.68 ± 0.72 dB, p&lt;0.05), which was consistent with 99m Tc-Sestamibi distribution findings. Myocardial perfusion defect areas assessed by both methods showed no differences and showed good correlation with Evans blue staining. ED frames were more favorable for imaging analysis. Conclusions: Both infusion and bolus administration of the contrast agent combined with RTMCE technique can provide a reliable and non-invasive approaches for myocardial perfusion assessment in rats, and the infusion method was more suitable for quantitative analysis of myocardial blood flow.

Contribution of magnetic resonance imaging in the differential diagnosis of cardiac amyloidosis and symmetric hypertrophic cardiomyopathy

Background Magnetic resonance imaging (MRI) provides a high-resolution study of atrial and ventricular myocardium depicting morphologic alterations in cardiomyopathies. Furthermore, in systemic amyloidosis, MRI demonstrates the capability to detect amyloid protein by tissue characterization. The aim of this study was to evaluate the potential of MRI in the diagnosis of cardiac amyloidosis. Methods MRI was performed in 16 patients with cardiac amyloidosis and in 10 patients with symmetric hypertrophic cardiomyopathy. Myocardial ventricular and atrial thickness (septum, posterior, and lateral wall), right and left ventricular diastolic diameter, and atrial surface were compared. Ventricular myocardium signal intensity was then evaluated by sequences with an echo time (TE) of 20 and 60 ms as the expression of myocardial texture modification. Results Significant morphologic differences between cardiac amyloidosis and hypertrophic cardiomyopathy were found in the right atrium surface (21.9 vs 17.2 cm 2 , respectively; P = .05), myocardial thickness of right atrial wall (9.3 vs 4.9 mm; P < .0001), and right ventricular free wall (10.6 vs 8.9 mm; P = .011). No significant differences were found in the interventricular septum (16.6 vs 17.8 mm), left ventricular posterior wall (18.2 vs 18.8 mm), and left atrial surface (17.4 vs 17.2 cm 2 ). The signal intensity of cardiac amyloidosis was significantly lower with both TE 20 and TE 60 in comparison with hypertrophic cardiomyopathy and to a group of healthy volunteers. Conclusions MRI has a potential role in the noninvasive diagnosis of cardiac amyloidosis identifying typical morphologic markers and suggesting the presence of infiltrative disease by tissue characterization. (Am Heart J 1998;136:824-30.)

929-65 Mechanisms of Hyperenhancement by Contrast Enhanced Magnetic Resonance Imaging are Related to Injured Myocardial Mass in Patients with Acute Myocardial Infarction

The extent of injured myocardium is directly related to infarct size after acute myocardial infarction (AMI). Myocardial hyperenhancement during ultrafast contrast enhanced magnetic resonance imaging (CEMRI) reflects ischemic injury and its mechanism; extracellular volume expansion with or without washout impairment may be related to the magnitude of ischemic injury; edema formation with or without cell death. To investigate the relationship between the extent of myocardial injury and the mechanism of myocardial hyperenhancement by CEMRI we studied 19 patients after AMI. Spoiled GRASS, TR = 6.5 ms, TE = 2.3 ms, 4 short-axis images were analyzed, and the ratio of signal intensity in myocardium to blood from injured (IN) and normal (NL) regions was obtained at 50 secs, 160 secs and 600 secs. after I.V contrast (gadoteridol 0.1 mmol/kg). Percent injured myocardial mass was calculated as the ratio of hyperenhanced myocardium to total LV mass by planimetry. Patients were divided into two groups according to the mechanism of signal hyperenhancement. Group 1 (N = 9) was defined by a parallel upwards displacement (ANOVA p &lt; 0.002) of the injured myocardiumlblood ratio over time relative to normal myocardium consistent with pure extracellular expansion. Group 2 (N = 111 had upwards displacement (ANOVA p &lt; 0,001) with significant slope (ANOVA p &lt; 0.001) consistent with impaired washout (see Figure). Injured mass was greater in Group 2 (31.9 ± 6.4%) than in Group 1(15.9 ± 5.0%, P &lt; 0.001). In conclusion, the mechanism of myocardial hyperenhancement is related to the extent of ischemic injury after AMI, with greater injury associated with the presence of washout impairment. suggesting cell death. These relationships may be explored to assess myocardial viability after AMI by CEMRI.