Aortic dissection in a young male with persistent ductus arteriosus and a novel variant in MYLK.

Pathogenic variants in several genes involved in the function or regulation of smooth muscle cells (SMC) are known to predispose to congenital heart disease and thoracic aortic aneurysm and dissection (TAAD). Variants in MYLK are primarily known to predispose to TAAD, but a growing body of evidence points toward MYLK also playing an essential role in the regulation of SMC contraction outside the aorta. In this case report, we present a patient with co-occurrence of persistent ductus arteriosus (PDA) and thoracic aortic dissection. Genetic analyses revealed a novel splice acceptor variant (c.3986-1G > A) in MYLK, which segregated with disease in the family. RNA-analyses on fibroblasts showed that the variant induced skipping of exon 24, which resulted in an in-frame deletion of 101 amino acids. These findings suggest that MYLK-associated disease could include a broader phenotypic spectrum than isolated TAAD, including PDA and obstructive pulmonary disease. Genetic analyses could be considered in families with TAAD and PDA or obstructive pulmonary disease.

National clinical Genetic Networks - GENets - Establishment of expert collaborations in Denmark.

Genetic conditions are often familial, but not all relatives receive counseling from the same institution. It is therefore necessary to ensure consistency in variant interpretation, counseling practices, and clinical follow up across health care providers. Furthermore, as new possibilities for gene-specific treatments emerge and whole genome sequencing becomes more widely available, efficient data handling and knowledge sharing between clinical laboratory geneticists and medical specialists in clinical genetics are increasingly important. In Denmark, these needs have been addressed through the establishment of collaborative national networks called Genetic Expert Networks or "GENets". These networks have enhanced patient and family care significantly by bringing together groups of experts in national collaborations. This promotes coordinated clinical care, the dissemination of best clinical practices, and facilitates the exchange of new knowledge.

Case report: A novel variant in SLC25A46 causing sensorimotor polyneuropathy and optic atrophy.

SLC25A46 is a mitochondrial protein involved in mitochondrial dynamics. Recently, bi-allelic variants have been identified as a pathogenic cause in a spectrum of neurological syndromes. We report a novel homozygous SLC25A46 variant in two siblings, originating from Iraq. Both presented with optic atrophy and varying neurological symptoms. The neurological examination and nerve conduction studies were consistent with sensorimotor polyneuropathy, one having mild polyneuropathy and the other pronounced polyneuropathy. The cases illustrate the disease spectrum and provide substantial information to the knowledge of polyneuropathy caused by SLC25A46 variants. It further highlights the diagnostic potentials of whole exome sequencing which can improve future understanding of disease mechanisms.

Myocardial fibrosis and ventricular ectopy in patients with non-ischemic systolic heart failure: results from the DANISH trial.

Patients with non-ischemic systolic heart failure (HF) have increased risk of sudden cardiovascular death (SCD). The initiation and substrate for ventricular arrhythmias remains poorly understood. Our purpose was to describe the relationship between cardiac magnetic resonance (CMR) late gadolinium enhancement (LGE) and Holter recorded ventricular arrhythmic activity. Patients from the DANISH trial underwent a Holter-recording and a CMR-scan. The presence of non-sustained ventricular tachycardia (NSVT) and premature ventricular contractions (PVC) were examined in relation to presence and amount of LGE. Outcome measures were all-cause mortality and SCD. Overall, 180 patients were included. LGE was present in 86 (47%). NSVT occurred in 72 (40%), not different according to LGE status (p = 0.65). The amount of LGE was not correlated to the occurrence of NSVT (p = 0.40). The occurrence of couplet PVCs (p = 0.997), frequent PVCs (p = 0.12), PVCs in bigemini (p = 0.29), in trigemini (p = 0.26), or in quadrimini (p = 0.35) did not differ according to LGE status. LGE was significantly associated with risk of all-cause mortality (HR 2.14; 95% CI 1.05-4.37, p = 0.04). NSVT did not increase risk of all-cause mortality in either patients with LGE (HR 1.00; 95% CI 0.46-2.16, p = 0.996) or without LGE (HR 1.37; 95% CI 0.46-4.08, p = 0.57). There was no interaction between LGE and NSVT for the risk of all-cause mortality (p = 0.62). In patients with non-ischemic systolic HF there was no relationship between the presence of LGE and NSVT or any other Holter recorded ventricular tachyarrhythmia. LGE was associated with increased risk of mortality, independent of the presence of NSVT.

[Genetic screening of adopted individuals].

Information regarding hereditary disease predisposition is generally inaccessible for adoptees. The lack of family history restricts access to various surveillance programmes and the overall health of the adoptee. Genetic screening of asymptomatic adoptees could be a compensational tool. However, variant classification is difficult, even more so in certain ethnic groups and in cases where there is no knowledge of family history, as summarised in this review. The usefulness of genetic screening of asymptomatic adoptees is still unknown and requires further research for clarification.

Myocardial fibrosis and the effect of primary prophylactic defibrillator implantation in patients with non-ischemic systolic heart failure-DANISH-MRI.

AIMS: Patients with non-ischemic systolic heart failure have an increased risk of sudden cardiac death (SCD). Myocardial fibrosis, detected as late gadolinium enhancement (LGE) with cardiac magnetic resonance (CMR), has been shown to predict all-cause mortality. We hypothesized that LGE can identify patients with non-ischemic heart failure who will benefit from ICD implantation. METHODS AND RESULTS: In this prospective observational sub-study of the Danish Study to Assess the Efficacy of ICDs in Patients with Nonischemic Systolic Heart Failure on Mortality (DANISH), 252 patients underwent CMR. LGE was quantified by the full width/half maximum method. The primary endpoint was all-cause mortality. LGE could be adequately assessed in 236 patients, median age was 61 years and median duration of heart failure was 14 months; there were 108 patients (46%) randomized to ICD. Median follow-up time was 5.3 years. Median left ventricular ejection fraction on CMR was 35%. In all, 50 patients died. LGE was present in 113 patients (48%). The presence of LGE was an independent predictor of all-cause mortality (HR 1.82; 95% CI 1.002-3.29; P = .049) after adjusting for known cardiovascular risk factors. ICD implantation did not impact all-cause mortality, for either patients with LGE (HR 1.18; 95% CI 0.59-2.38; P = .63), or for patients without LGE (HR 1.00; 95% CI 0.39-2.53; P = .99), (P for interaction =0.79). CONCLUSION: In patients with non-ischemic systolic heart failure, LGE predicted all-cause mortality. However, in this cohort, LGE did not identify a group of patients who survived longer by receiving an ICD.

Right Ventricular Dysfunction and the Effect of Defibrillator Implantation in Patients With Nonischemic Systolic Heart Failure.

Background Patients with nonischemic systolic heart failure are at an increased risk of sudden cardiac death, but more discriminating tools are needed to identify those patients likely to benefit from implantable cardioverter-defibrillator (ICD) implantation. Whether right ventricular (RV) ejection fraction (RVEF) can identify patients with nonischemic systolic heart failure more likely to benefit from ICD implantation is not yet known. Methods In this post hoc analysis of the DANISH trial (Danish Study to Assess the Efficacy of ICDs in Patients with Nonischemic Systolic Heart Failure on Mortality), patients with nonischemic systolic heart failure randomized to ICD or control underwent cardiovascular magnetic resonance. RV systolic dysfunction was defined as RVEF ≤45%. Cox regression assessed the effects of RV function and ICD implantation on all-cause mortality, sudden cardiac death, and cardiovascular death. Results Overall, 239 patients had interpretable images of RV volume. Median RVEF was 51%, RV systolic dysfunction was present in 75 (31%) patients, and 55 (23%) patients died. RVEF was an independent predictor of all-cause mortality, hazards ratio 1.34 per 10% absolute decrease in RVEF (95% CI, 1.05-1.70), P=0.02. There was a statistically significant interaction between RVEF and the effect of ICD implantation ( P=0.001). ICD implantation significantly reduced all-cause mortality in patients with RV systolic dysfunction, hazards ratio 0.41 (95% CI, 0.17-0.97), P=0.04 but not in patients without RV systolic dysfunction, hazards ratio 1.87 (95% CI, 0.85-3.92), P=0.12, ( P=0.01 for the difference in effect of ICD between RV groups). Conclusions In this post hoc analysis of the DANISH trial, ICD therapy was associated with survival benefit in patients with biventricular heart failure. These findings need confirmation in a prospective study. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov . Unique identifier: NCT00542945.

Early Gadolinium Enhancement for Determination of Area at Risk: A Preclinical Validation Study.

OBJECTIVES: The aim of this study was to determine whether early gadolinium enhancement (EGE) by cardiac magnetic resonance (CMR) in a canine model of reperfused myocardial infarction depicts the area at risk (AAR) as determined by microsphere blood flow analysis. BACKGROUND: It remains controversial whether only the irreversibly injured myocardium enhances when CMR is performed in the setting of acute myocardial infarction. Recently, EGE has been proposed as a measure of the AAR in acute myocardial infarction because it correlates well with T2-weighted imaging of the AAR, but this still requires pathological validation. METHODS: Eleven dogs underwent 2 h of coronary artery occlusion and 48 h of reperfusion before imaging at 1.5-T. EGE imaging was performed 3 min after contrast administration with coverage of the entire left ventricle. Late gadolinium enhancement imaging was performed between 10 and 15 min after contrast injection. AAR was defined as myocardium with blood flow <2 SD from remote myocardium determined by microspheres during occlusion. The size of infarction was determined with triphenyltetrazolium chloride. RESULTS: There was no significant difference in the size of enhancement by EGE compared with the size of AAR by microspheres (44.1 ± 15.8% vs. 42.7 ± 9.2%; p = 0.61), with good correlation (r = 0.88; p < 0.001) and good agreement by Bland-Altman analysis (mean bias 1.4 ± 17.4%). There was no difference in the size of enhancement by EGE compared with enhancement on native T1 and T2 maps. The size of EGE was significantly greater than the infarct by triphenyltetrazolium chloride (44.1 ± 15.8% vs. 20.7 ± 14.4%; p < 0.001) and late gadolinium enhancement (44.1 ± 15.8% vs. 23.5 ± 12.7%; p < 0.001). CONCLUSIONS: At 3 min post-contrast, EGE correlated well with the AAR by microspheres and CMR and was greater than infarct size. Thus, EGE enhances both reversibly and irreversibly injured myocardium.

Mechanisms for overestimating acute myocardial infarct size with gadolinium-enhanced cardiovascular magnetic resonance imaging in humans: a quantitative and kinetic study.

AIMS: It remains controversial whether cardiovascular magnetic resonance imaging with gadolinium only enhances acutely infarcted or also salvaged myocardium. We hypothesized that enhancement of salvaged myocardium may be due to altered extracellular volume (ECV) and contrast kinetics compared with normal and infarcted myocardium. If so, these mechanisms could contribute to overestimation of acute myocardial infarction (AMI) size. METHODS AND RESULTS: Imaging was performed at 1.5T ≤ 7 days after AMI with serial T1 mapping and volumetric early (5 min post-contrast) and late (20 min post-contrast) gadolinium enhancement imaging. Infarcts were classified as transmural (>75% transmural extent) or non-transmural. Patients with non-transmural infarctions (n = 15) had shorter duration of symptoms before reperfusion (P = 0.02), lower peak troponin (P = 0.008), and less microvascular obstruction (P < 0.001) than patients with transmural infarcts (n = 22). The size of enhancement at 5 min was greater than at 20 min (18.7 ± 12.7 vs. 12.1 ± 7.0%, P = 0.003) in non-transmural infarctions, but similar in transmural infarctions (23.0 ± 10.0 vs. 21.9 ± 9.9%, P = 0.21). ECV of salvaged myocardium was greater than normal (39.5 ± 5.8 vs. 24.1 ± 3.1%) but less than infarcted myocardium (50.5 ± 6.0%, both P < 0.001). In kinetic studies of non-transmural infarctions, salvaged and infarcted myocardium had similar T1 at 4 min but different T1 at 8-20 min post-contrast. CONCLUSION: The extent of gadolinium enhancement in AMI is modulated by ECV and contrast kinetics. Image acquisition too early after contrast administration resulted in overestimation of infarct size in non-transmural infarctions due to enhancement of salvaged myocardium.

Characterization of myocardial T1-mapping bias caused by intramyocardial fat in inversion recovery and saturation recovery techniques.

BACKGROUND: Quantitative measurement of T1 in the myocardium may be used to detect both focal and diffuse disease processes such as interstitial fibrosis or edema. A partial volume problem exists when a voxel in the myocardium also contains fat. Partial volume with fat occurs at tissue boundaries or within the myocardium in the case of lipomatous metaplasia of replacement fibrosis, which is commonly seen in chronic myocardial infarction. The presence of fat leads to a bias in T1 measurement. The mechanism for this artifact for widely used T1 mapping protocols using balanced steady state free precession readout and the dependence on off-resonance frequency are described in this paper. METHODS: Simulations were performed to illustrate the behavior of mono-exponential fitting to bi-exponential mixtures of myocardium and fat with varying fat fractions. Both inversion recovery and saturation recovery imaging protocols using balanced steady state free precession are considered. In-vivo imaging with T1-mapping, water/fat separated imaging, and late enhancement imaging was performed on subjects with chronic myocardial infarction. RESULTS: In n = 17 subjects with chronic myocardial infarction, lipomatous metaplasia is evident in 8 patients (47%). Fat fractions as low as 5% caused approximately 6% T1 elevation for the out-of-phase condition, and approximately 5% reduction of T1 for the in-phase condition. T1 bias in excess of 1000 ms was observed in lipomatous metaplasia with fat fraction of 38% in close agreement with simulation of the specific imaging protocols. CONCLUSIONS: Measurement of the myocardial T1 by widely used balanced steady state free precession mapping methods is subject to bias when there is a mixture of water and fat in the myocardium. Intramyocardial fat is frequently present in myocardial scar tissue due lipomatous metaplasia, a process affecting myocardial infarction and some non-ischemic cardiomyopathies. In cases of lipomatous metaplasia, the T1 biases will be additive or subtractive depending on whether the center frequency corresponds to the myocardium and fat being in-phase or out-of-phase, respectively. It is important to understand this mechanism, which may otherwise lead to erroneous interpretation.

Temporal and spatial characteristics of the area at risk investigated using computed tomography and T1-weighted magnetic resonance imaging.

AIMS: Cardiovascular magnetic resonance (CMR) imaging can measure the myocardial area at risk (AAR), but the technique has received criticism for inadequate validation. CMR commonly depicts an AAR that is wider than the infarct, which in turn would require a lateral perfusion gradient within the AAR. We investigated the presence of a lateral perfusion gradient within the AAR and validated CMR measures of AAR against three independent reference standards of high quality. METHODS AND RESULTS: Computed tomography (CT) perfusion imaging, microsphere blood flow analysis, T1-weighted 3T CMR and fluorescent microparticle pathology were used to investigate the AAR in a canine model (n = 10) of ischaemia and reperfusion. AAR size by CMR correlated well with CT (R(2) = 0.80), microsphere blood flow (R(2) = 0.80), and pathology (R(2) = 0.74) with good limits of agreement [-0.79 ± 4.02% of the left ventricular mass (LVM) vs. CT; -1.49 ± 4.04% LVM vs. blood flow and -1.01 ± 4.18% LVM vs. pathology]. The lateral portion of the AAR had higher perfusion than the core of the AAR by CT perfusion imaging (40.7 ± 11.8 vs. 25.2 ± 17.7 Hounsfield units, P = 0.0008) and microsphere blood flow (0.11 ± 0.04 vs. 0.05 ± 0.02 mL/g/min, lateral vs. core, P = 0.001). The transmural extent of MI was lower in the lateral portion of the AAR than the core (28.2 ± 10.2 vs. 17.4 ± 8.4% of the wall, P = 0.001). CONCLUSION: T1-weighted CMR accurately quantifies size of the AAR with excellent agreement compared with three independent reference standards. A lateral perfusion gradient results in lower transmural extent of infarction at the edges of the AAR compared with the core.

Distinction of salvaged and infarcted myocardium within the ischaemic area-at-risk with T2 mapping.

AIM: Area-at-risk (AAR) measurements often rely on T2-weighted images, but subtle differences in T2 may be overlooked with this method. To determine the differences in oedema between salvaged and infarcted myocardium, we performed quantitative T2 mapping of the AAR. We also aimed to determine the impact of reperfusion time on T2 in the AAR. METHODS: Twenty-two dogs underwent 2 h of coronary occlusion followed by 4 or 48 h of reperfusion before cardiac magnetic resonance imaging at 1.5 T. Late gadolinium enhancement images were used to define the infarcted, salvaged, and remote myocardium. T2 values from T2 maps and signal intensities on T2-weighted images were measured in the corresponding areas. RESULTS: At both imaging time points, the T2 of the salvaged myocardium was longer than of remote (66.0 ± 6.9 vs. 51.4 ± 3.5 ms, P < 0.001 at 4 h, and 56.7 ± 7.3 vs. 48.1 ± 3.5 ms, P < 0.001 at 48 h). The T2 was also longer in the infarcted myocardium compared with remote at both 4 and 48 h (71.4 ± 7.6 ms, P < 0.01 vs. salvage and 64.0 ± 6.9 ms, P = 0.03 vs. salvage, both P < 0.001 vs. remote). The increase in T2 in the salvaged myocardium compared with remote was greater after 4 h than after 48 h (14.7 ± 5.6 vs. 8.7 ± 5.1 ms, P = 0.02). CONCLUSIONS: T2 relaxation parameters are different in the infarcted and salvaged myocardium, and both are significantly longer than remote. Furthermore, the magnitude of increase in T2 was less in the salvaged myocardium after longer reperfusion, indicating partial resolution of oedema in the first 48 h after reperfusion.

Differences in cardiovascular risk profile between electrocardiographic hypertrophy versus strain in asymptomatic patients with aortic stenosis (from SEAS data).

Electrocardiograms are routinely obtained in clinical follow-up of patients with asymptomatic aortic stenosis (AS). The association with aortic valve, left ventricular (LV) response to long-term pressure load, and clinical covariates is unclear and the clinical value is thus uncertain. Data from clinical examination, electrocardiogram, and echocardiogram in 1,563 patients in the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study were used. Electrocardiograms were Minnesota coded for arrhythmias and atrioventricular and intraventricular blocks; LV hypertrophy was assessed by Sokolow-Lyon voltage and Cornell voltage-duration criteria; and strain by T-wave inversion and ST-segment depression. Degree of AS severity was evaluated by echocardiography as peak aortic jet velocity and LV mass was indexed by body surface area. After adjustment for age, gender, LV mass index, heart rate, systolic and diastolic blood pressures, blood glucose, digoxin, antiarrhythmic drugs, drugs acting on the renin-angiotensin system, diuretics, ß blockers and calcium receptor blockers; peak aortic jet velocity was significantly greater in patients with electrocardiographic strain (mean difference 0.13 m/s, p <0.001) and LV hypertrophy by Sokolow-Lyon voltage criteria (mean difference 0.12 m/s, p = 0.004). After similar adjustment, LV mass index was significantly greater in patients with electrocardiographic strain (mean difference 14.8 g/cm(2), p <0.001) and LV hypertrophy by Sokolow-Lyon voltage criteria and Cornell voltage-duration criteria (mean differences 8.8 and 17.8 g/cm(2), respectively, p <0.001 for the 2 comparisons). In multiple comparisons patients with electrocardiographic strain had increased peak aortic jet velocity, blood glucose, and uric acid, whereas patients with LV hypertrophy by Sokolow-Lyon voltage criteria were younger and patients with LV hypertrophy by Cornell voltage-duration criteria more often were women. In conclusion, electrocardiographic criteria for LV hypertrophy and strain are independently associated with peak aortic jet velocity and LV mass index. Moreover, clinical covariates differ significantly between patients with electrocardiographic strain and those with LV hypertrophy by Sokolow-Lyon voltage criteria and Cornell voltage-duration criteria.

Determinants of exercise-induced increase of mitral regurgitation in patients with acute coronary syndromes.

BACKGROUND: Mechanisms behind exercise-induced increase of mitral regurgitation (MR) in patients with chronic ischemic heart disease have been described earlier. We describe the determinants of exercise-induced changes in MR in patients with non-ST-elevation acute coronary syndrome (NSTACS). METHODS: Forty-five consecutive patients (mean + or - SD age 64 + or - 10 years, 37 men) with NSTACS underwent exercise echocardiography on a supine bicycle the day before angiography. The exercise was started with a load of 10 W with increments of 10 W every minute until symptoms developed or a max load of 100 W. Effective regurgitation orifice (ERO) was measured at rest and at peak exercise. RESULTS: Twelve patients had more than trace MR at rest with ERO 8 + or - 5 (mean + or - SD), range: 3-18 mm(2). In these patients, ERO increased during exercise to 13 + or - 6 (mean + or - SD), range: 6-23 mm(2) corresponding to an increase of 70% from rest (P = 0.001). Seven other patients developed new MR during exercise with ERO at peak exercise of 8 + or - 4 mm(2) (mean + or - SD), range: 4-14 mm(2). All these patients had significant increase in wall motion score index (WMSI) of 0.14 + or - 0.18 (mean + or - SD), P = 0.006, while in the 25 patients without MR at rest or during exercise, WMSI remained unchanged, -0.02 + or - 0.08 (mean + or - SD), P = 0.2. CONCLUSION: Exercise-induced increases of MR in patients with NSTACS are related to worsening of regional wall motions. (Echocardiography 2010;27:567-574).

Assessment of left atrial volume and mechanical function in ischemic heart disease: a multi slice computed tomography study.

UNLABELLED: Left atrial (LA) maximal volume contains prognostic information in patients with heart failure and acute myocardial infarction. However, only few studies have investigated the detailed mechanical function of the LA in these patients. We assessed the feasibility of evaluating LA volume and mechanical function with Multi Slice Computed Tomography (MSCT) in patients with ischemic heart disease. Furthermore, the LA and left ventricular (LV) function was evaluated in relation to signs of clinical heart failure. METHODS AND RESULTS: MSCT was performed in 40 patients with sinus rhythm and ischemic heart disease. We enrolled 20 patients with reduced LV ejection fraction (LVEF≤45%) and 20 with preserved LVEF (>45%). LA volumes, reservoir, channel and pump function were measured. Interobserver variation for LA volume measures was 1.5% (SD: 6.6%). In patients with reduced LVEF, LA volumes were larger throughout the cardiac cycle (LA-max 66.8 ml/m(2) vs 57.4 ml/m(2) and LA-min: 45.8 ml/m(2) vs 31.6 ml/m(2), p<0.05) and LA reservoir and pump function were all significantly impaired (Fractional change: 43% vs 31%, LAEF 31% vs 19%, p<0.05). Patients with clinical signs of heart failure during hospitalisation had significantly lower LAEF than patients without (16(9)% vs. 30(17)% p<0.05). In a multivariate linear regression analyses the presence of clinical signs of heart failure and reduced LVEF were independent determinants of impaired LA reservoir and pump function (p<0.05). CONCLUSION: Reproducible assessment of LA size and mechanical function throughout the cardiac cycle using MSCT is feasible and potentially useful clinically.

Volumetric evaluation of coronary plaque in patients presenting with acute myocardial infarction or stable angina pectoris-a multislice computerized tomography study.

BACKGROUND: We hypothesized that unstable clinical presentation of coronary artery disease is associated with distinct characteristics of culprit lesions identifiable by multislice computed tomography (MSCT). METHODS: Patients with non-ST-elevation myocardial infarction (NSTEMI) (n = 57) or stable angina (SA) pectoris (n = 19) were studied. Coronary culprit lesions in patients with NSTEMI and symptomatic lesions in patients with SA were evaluated with 64-slice MSCT and a volumetric plaque imaging tool. Plaque volumes of lipid, fibrous tissue, or calcification according to signal intensity were determined. Plaque burden, mean signal intensity of the lesions, relative volumetric distribution of plaque components, and remodeling index were measured. RESULTS: Volumetric plaque burden of study lesions were similar in the 2 patient groups (P = .38). Mean signal intensity of study lesions were lower in patients with NSTEMI compared with patients with SA (74 [66-97] Hounsfield units vs 99 [77-154] Hounsfield units, P = .02). The volume of plaque occupied by calcified material was lower in patients with NSTEMI compared with patients with SA (15 mm(3) [3-58 mm(3)] vs 42 mm(3) [18-82 mm(3)], P = .045). In patients with NSTEMI, the lipid-rich plaque subtype was more frequent than in patients with SA, and the calcified plaque subtype was less frequent in patients with NSTEMI than in patients with SA (P = .032). Positive remodeling was observed in 19% of patients with NSTEMI, whereas this was absent in patients with SA (P = .04). CONCLUSION: Volumetric measurements with MSCT revealed that coronary culprit lesions in acute coronary syndrome frequently display low mean plaque signal intensity values, lipid-rich plaque subtype, and positive remodeling.