Intramyocardial Fat Research Articles

Association of epicardial adipose tissue with cardiac geometry alternation and diastolic dysfunction in the early stage of diabetic cardiomyopathy

Abstract Background Diastolic dysfunction and alterations in cardiac geometry are early indicators of diabetic cardiomyopathy. However, the association between cardiac changes across the glucose continuum and the contribution of epicardial adipose tissue (EAT) to these changes has not yet been investigated. Purpose In this study, we aim to investigated the EAT on cardiac diastolic function and structural alterations along the diabetic continuum using cardiac magnetic resonance imaging (CMR). Methods We enrolled individuals who were categorized into groups based on glucose tolerance status. Left ventricular structure and diastolic function were assessed using echocardiography and CMR to determine the EAT, intramyocardial fat, and associated parameters. Multivariate logistic regression models were also used. Results In a study of 370 patients (209 normal glucose tolerance, 82 prediabetes, 79 diabetes), those with prediabetes and diabetes showed increased heart dimensions and diastolic dysfunction, including E/E' (7.9±0.51 vs. 8.5±0.64 vs. 10.0±0.93, p=0.010), left atrial volume index (28.21±14.7 vs. 33.2±12.8 vs. 37.4±8.2 mL/m2, p<0.001), and left ventricular peak filling rate (4.46±1.75 vs. 3.61±1.55 vs. 3.20±1.30 mL/s, p<0.001). EAT significantly increased in prediabetes and diabetes (26.3±1.16 vs. 31.3±1.83 vs. 33.9±1.9 gm, p=0.001), while intramyocardial fat did not differ significantly. Prediabetes altered heart geometry, but not diastolic function (OR 1.22 [1.02–1.83], p=0.012; and 1.70 [0.79–3.68], p=0.135). Diabetes significantly affected both heart structure and diastolic function (OR 1.42 [1.11–1.97], p=0.032; and 2.56 [1.03–5.40], p=0.034) after adjusting for covariates. Conclusions Elevated EAT was observed in patients with prediabetes and is associated with adverse alterations in cardiac structure and diastolic function, potentially serving as an underlying mechanism for the early onset of diabetic cardiomyopathy.

Lipomatous Metaplasia Facilitates Ventricular Tachycardia in Patients WithNonischemic Cardiomyopathy.

Ventricular tachycardia (VT) substrate in patients with nonischemic cardiomyopathy (NICM) is complex in distribution and intramural location. This study sought to test the hypothesis that myocardial lipomatous metaplasia (LM) is a vital anatomic substrate for VT corridors in patients with NICM and VT, and that LM stabilizes current propagation in VT corridors. Among 49 patients with NICM in the 2-center INFINITY (Prospective Intra-Myocardial Fat Deposition and Ventricular Tachycardia in Cardiomyopathy) Study, potential VT viable corridors within the myocardial scar and/or LM were computed from late gadolinium enhancement cardiac magnetic resonance images and were registered with electroanatomical maps. Corridors passing through VT entrance, isthmus, and/or exit sites, estimated by entrainment or pace mapping, were defined as VT corridors. LM was separately distinguished from scar using computed tomography. The SD of current amplitude along each corridor was measured. Compared with 151 non-VT corridors, 35 VT corridors traversed a substantially higher volume of LM, with a median 236.6mg (IQR: 13.5-903.4mg) vs 5.8mg (IQR: 0.0-57.9mg) (P< 0.001). Among corridors with computable current amplitude, 28 VT corridors exhibited substantially lower current variation along the corridors, with SD 8.0 μA (25th-75th percentile: 6.1-10.3 μA) vs 14.9 μA (25th-75th percentile: 8.5-23.7 μA) among 71 non-VT corridors (P<0.001). Individual VT circuit sites (95 out 118) were highly colocalized with LM. VT circuitry corridors in NICM are more likely to traverse LM and exhibit reduced current amplitude variation compared with bystander corridors.

Sexual dimorphism in the relationships between intramyocardial fat, myocardial fibrosis, and exercise intolerance in heart failure with preserved ejection fraction.

Sexual dimorphism in the relationships between intramyocardial fat, myocardial fibrosis, and exercise intolerance in heart failure with preserved ejection fraction.

Epicardial Adipose Tissue is Associated with Geometry Alteration and Diastolic Dysfunction in Prediabetic Cardiomyopathy.

Diastolic dysfunction and alterations in cardiac geometry are early indicators of diabetic cardiomyopathy. However, the association between cardiac changes across the glucose continuum and the contribution of epicardial adipose tissue (EAT) to these changes has not yet been investigated. In this study, we aim to investigated the EAT on cardiac diastolic function and structural alterations along the diabetic continuum using cardiac magnetic resonance imaging (CMRI). We enrolled individuals who were categorized into groups based on glucose tolerance status. Left ventricular structure and diastolic function were assessed using echocardiography and CMRI to determine the EAT, intramyocardial fat, and associated parameters. Multivariable logistic regression models were also used. In a study of 370 patients (209 normal glucose tolerance, 82 prediabetes, 79 diabetes), those with prediabetes and diabetes showed increased heart dimensions and diastolic dysfunction, including E/E' (the ratio of early mitral inflow velocity to mitral annular early diastolic velocity) (7.9±0.51 vs. 8.5±0.64 vs. 10.0±0.93, p=0.010), left atrial volume index (28.21±14.7 vs. 33.2±12.8 vs. 37.4±8.2 mL/m2, p<0.001), and left ventricular peak filling rate (4.46±1.75 vs. 3.61±1.55 vs. 3.20±1.30 mL/s, p<0.001). EAT significantly increased in prediabetes and diabetes (26.3±1.16 vs. 31.3±1.83 vs. 33.9±1.9 gm, p=0.001), while intramyocardial fat did not differ significantly. Prediabetes altered heart geometry, but not diastolic function (OR 1.22 [1.02-1.83], p=0.012; and 1.70 [0.79-3.68], p=0.135). Diabetes significantly affected both heart structure and diastolic function (OR 1.42 [1.11-1.97], p=0.032; and 2.56 [1.03-5.40], p=0.034) after adjusting for covariates. Elevated EAT was observed in patients with prediabetes and is associated with adverse alterations in cardiac structure and diastolic function, potentially serving as an underlying mechanism for the early onset of diabetic cardiomyopathy.

Assessing left atrial intramyocardial fat infiltration from computerized tomography angiography in patients with atrial fibrillation.

Epicardial adipose tissue might promote atrial fibrillation (AF) in several ways, including infiltrating the underlying atrial myocardium. However, the role of this potential mechanism has been poorly investigated. The aim of this study is to evaluate the presence of left atrial (LA) infiltrated adipose tissue (inFAT) by analysing multi-detector computer tomography (MDCT)-derived three-dimensional (3D) fat infiltration maps and to compare the extent of LA inFAT between patients without AF history, with paroxysmal, and with persistent AF. Sixty consecutive patients with AF diagnosis (30 persistent and 30 paroxysmal) were enrolled and compared with 20 age-matched control; MDCT-derived images were post-processed to obtain 3D LA inFAT maps for all patients. Volume (mL) and mean signal intensities [(Hounsfield Units (HU)] of inFAT (HU -194; -5), dense inFAT (HU -194; -50), and fat-myocardial admixture (HU -50; -5) were automatically computed by the software. inFAT volume was significantly different across the three groups (P = 0.009), with post-hoc pairwise comparisons showing a significant increase in inFAT volume in persistent AF compared to controls (P = 0.006). Dense inFAT retained a significant difference also after correcting for body mass index (P = 0.028). In addition, more negative inFAT radiodensity values were found in AF patients. Regional distribution analysis showed a significantly higher regional distribution of LA inFAT at left and right superior pulmonary vein antra in AF patients. Persistent forms of AF are associated with greater degree of LA intramyocardial adipose infiltration, independently of body mass index. Compared to controls, AF patients present higher LA inFAT volume at left and right superior pulmonary vein antra.

Abstract 12905: Epicardial and Intramyocardial Fat as Predictors of Ventricular Arrhythmia in Ischemic and Non-Ischemic Cardiomyopathy

Background: Sudden cardiac death from ventricular arrhythmia (VA) is a global concern. While emerging evidence suggests a role for myocardial fat in the development of VA among ischemic (ICM) and non-ischemic cardiomyopathy (NICM) patients, the volume and distribution of epicardial adipose tissue (EAT) and intramyocardial fat (IMF) linked to VA remain underexplored. Objective: To evaluate the predictive value of LV tissue heterogeneity, EAT, and IMF volumes in assessing the risk of VA in ICM and NICM patients. Methods: Patients enrolled in the PROSE-ICD registry, who underwent contrast-enhanced computed tomography were included. The designated endpoint was ventricular arrhythmia, defined as appropriate ICD shock or sudden arrhythmic death. IMF volume (voxels between -180 and -5 HU), EAT volume (voxels between -200 to -50 HU), and myocardial fat tissue heterogeneity (defined as the magnitude of change between nearby voxels) were calculated. Logistic regression models were employed to assess the association between explanatory variables and outcome. Results: 98 patients (47 ICM, 51 NICM) were included with a mean follow up time of 5.6±3.4 years. Participants’ mean age was 56±13.2 years, and 66% were male. LV tissue heterogeneity (per HU/mm) was associated with VA incidence (OR = 1.11; P &lt; 0.01) in the ICM cohort, whereas EAT and IMF volume were associated with VA in the NICM subgroup [(OR = 1.12; P &lt; 0.01), and (OR = 1.21; P = 0.01), respectively]. Even after adjusting for various covariates, LV tissue heterogeneity in the ICM group and EAT in the NICM group maintained a significant association with VA. Conclusion: In ICM, increased fat distribution heterogeneity is associated with VA, while in NICM, increased IMF and EAT volume are linked to a higher risk for VA. These findings suggest that LV tissue heterogeneity and EAT volume offer valuable prognostic insights in cardiomyopathy patients, indicating that the contribution of fat to VA depends on the underlying substrate.

How intramyocardial fat can alter the electric field distribution during Pulsed Field Ablation (PFA): Qualitative findings from computer modeling.

Even though the preliminary experimental data suggests that cardiac Pulsed Field Ablation (PFA) could be superior to radiofrequency ablation (RFA) in terms of being able to ablate the viable myocardium separated from the catheter by collagen and fat, as yet there is no formal physical-based analysis that describes the process by which fat can affect the electric field distribution. Our objective was thus to determine the electrical impact of intramyocardial fat during PFA by means of computer modeling. Computer models were built considering a PFA 3.5-mm blunt-tip catheter in contact with a 7-mm ventricular wall (with and without a scar) and a 2-mm epicardial fat layer. High voltage was set to obtain delivered currents of 19, 22 and 25 A. An electric field value of 1000 V/cm was considered as the lethal threshold. We found that the presence of fibrotic tissue in the scar seems to have a similar impact on the electric field distribution and lesion size to that of healthy myocardium only. However, intramyocardial fat considerably alters the electrical field distribution and the resulting lesion shape. The electric field tends to peak in zones with fat, even away from the ablation electrode, so that 'cold points' (i.e. low electric fields) appear around the fat at the current entry and exit points, while 'hot points' (high electric fields) occur in the lateral areas of the fat zones. The results show that intramyocardial fat can alter the electric field distribution and lesion size during PFA due to its much lower electrical conductivity than that of myocardium and fibrotic tissue.

Association of epicardial and intramyocardial fat with ventricular arrhythmias

Among patients with ischemic cardiomyopathy (ICM) and nonischemic cardiomyopathy (NICM), myocardial fibrosis is associated with an increased risk for ventricular arrhythmia (VA). Growing evidence suggests that myocardial fat contributes to ventricular arrhythmogenesis. However, little is known about the volume and distribution of epicardial adipose tissue and intramyocardial fat and their relationship with VAs. The purpose of this study was to assess the association of contrast-enhanced computed tomography (CE-CT)-derived left ventricular (LV) tissue heterogeneity, epicardial adipose tissue volume, and intramyocardial fat volume with the risk of VA in ICM and NICM patients. Patients enrolled in the PROSE-ICD registry who underwent CE-CT were included. Intramyocardial fat volume (voxels between -180 and -5 Hounsfield units [HU]), epicardial adipose tissue volume (between -200 and -50 HU), and LV tissue heterogeneity were calculated. The primary endpoint was appropriate ICD shocks or sudden arrhythmic death. Among 98 patients (47 ICM, 51 NICM), LV tissue heterogeneity was associated with VA (odds ratio [OR] 1.10; P = .01), particularly in the ICM cohort. In the NICM subgroup, epicardial adipose tissue and intramyocardial fat volume were associated with VA (OR 1.11, P = .01; and OR = 1.21, P = .01, respectively) but not in the ICM patients (OR 0.92, P =.22; and OR = 0.96, P =.19, respectively). In ICM patients, increased fat distribution heterogeneity is associated with VA. In NICM patients, an increased volume of intramyocardial fat and epicardial adipose tissue is associated with a higher risk for VA. Our findings suggest that fat's contribution to VAs depends on the underlying substrate.

Lipomatous Metaplasia Facilitates Slow Conduction in Critical Ventricular Tachycardia Corridors Within Postinfarct Myocardium

BackgroundMyocardial lipomatous metaplasia (LM) has been reported to be associated with post-infarct ventricular tachycardia (VT) circuitry. ObjectivesThis study examined the association of scar versus LM composition with impulse conduction velocity (CV) in putative VT corridors that traverse the infarct zone in post-infarct patients. MethodsThe cohort included 31 post-infarct patients from the prospective INFINITY (Intra-Myocardial Fat Deposition and Ventricular Tachycardia in Cardiomyopathy) study. Myocardial scar, border zone, and potential viable corridors were defined by late gadolinium enhancement cardiac magnetic resonance (LGE-CMR), and LM was defined by computed tomography. Images were registered to electroanatomic maps, and the CV at each electroanatomic map point was calculated as the mean CV between that point and 5 adjacent points along the activation wave front. ResultsRegions with LM exhibited lower CV than scar (median = 11.9 vs 13.5 cm/s; P < 0.001). Of 94 corridors computed from LGE-CMR and electrophysiologically confirmed to participate in VT circuitry, 93 traversed through or near LM. These critical corridors displayed slower CV (median 8.8 [IQR: 5.9-15.7] cm/s vs 39.2 [IQR: 28.1-58.5]) cm/s; P < 0.001) than 115 noncritical corridors distant from LM. Additionally, critical corridors demonstrated low-peripheral, high-center (mountain shaped, 23.3%) or mean low-level (46.7%) CV patterns compared with 115 noncritical corridors distant from LM that displayed high-peripheral, low-center (valley shaped, 19.1%) or mean high-level (60.9%) CV patterns. ConclusionsThe association of myocardial LM with VT circuitry is at least partially mediated by slowing nearby corridor CV thus facilitating an excitable gap that enables circuit re-entry.

Lipomatous metaplasia prolongs repolarization and increases repolarization dispersion within post-infarct ventricular tachycardia circuit cites.

Post-infarct myocardium contains viable corridors traversing scar or lipomatous metaplasia (LM). Ventricular tachycardia (VT) circuitry has been separately reported to associate with corridors that traverse LM and with repolarization heterogeneity. We examined the association of corridor activation recovery interval (ARI) and ARI dispersion with surrounding tissue type. The cohort included 33 post-infarct patients from the prospective Intra-Myocardial Fat Deposition and Ventricular Tachycardia in Cardiomyopathy (INFINITY) study. We co-registered scar and corridors from late gadolinium enhanced magnetic resonance, and LM from computed tomography with intracardiac electrogram locations. Activation recovery interval was calculated during sinus or ventricular pacing, as the time interval from the minimum derivative within the QRS to the maximum derivative within the T-wave on unipolar electrograms. Regional ARI dispersion was defined as the standard deviation (SD) of ARI per AHA segment (ARISD). Lipomatous metaplasia exhibited higher ARI than scar [325 (interquartile range 270-392) vs. 313 (255-374), P < 0.001]. Corridors critical to VT re-entry were more likely to traverse through or near LM and displayed prolonged ARI compared with non-critical corridors [355 (319-397) vs. 302 (279-333) ms, P < 0.001]. ARISD was more closely associated with LM than with scar (likelihood ratio χ2 50 vs. 12, and 4.2-unit vs. 0.9-unit increase in 0.01*Log(ARISD) per 1 cm2 increase per AHA segment). Additionally, LM and scar exhibited interaction (P < 0.001) in their association with ARISD. Lipomatous metaplasia is closely associated with prolonged local action potential duration of corridors and ARI dispersion, which may facilitate the propensity of VT circuit re-entry.

Native T1 Mapping for the Diagnosis of Myocardial Fibrosis in Patients With Chronic Myocardial Infarction

BackgroundMyocardial fibrosis is a fundamental process in cardiac injury. Cardiac magnetic resonance native T1 mapping has been proposed for diagnosing myocardial fibrosis without the need for gadolinium contrast. However, recent studies suggest that T1 measurements can be erroneous in the presence of intramyocardial fat. ObjectivesThe purpose of this study was to investigate whether the presence of fatty metaplasia affects the accuracy of native T1 maps for the diagnosis of myocardial replacement fibrosis in patients with chronic myocardial infarction (MI). MethodsConsecutive patients (n = 312) with documented chronic MI (>6 months old) and controls without MI (n = 50) were prospectively enrolled. Presence and size of regions with elevated native T1 and infarction were quantitatively determined (mean + 5SD) on modified look-locker inversion-recovery and delayed-enhancement images, respectively, at 3.0-T. The presence of fatty metaplasia was determined using an out-of-phase steady-state free-precession cine technique and further verified with standard fat-water Dixon methods. ResultsNative T1 mapping detected chronic MI with markedly higher sensitivity in patients with fatty metaplasia than those without fatty metaplasia (85.6% vs 13.3%) with similar specificity (100% vs 98.9%). In patients with fatty metaplasia, the size of regions with elevated T1 significantly underestimated infarct size and there was a better correlation with fatty metaplasia size than infarct size (r = 0.76 vs r = 0.49). In patients without fatty metaplasia, most of the modest elevation in T1 appeared to be secondary to subchronic infarcts that were 6 to 12 months old; the T1 of infarcts >12 months old was not different from noninfarcted myocardium. ConclusionsNative T1 mapping is poor at detecting replacement fibrosis but may indirectly detect chronic MI if there is associated fatty metaplasia. Native T1 mapping for the diagnosis and characterization of myocardial fibrosis is unreliable.

Abstract 12655: Lipomatous Metaplasia in Chronic Infarcts is Associated With Prolonged Activation Recovery Interval Within Ventricular Tachycardia Corridors

Introduction: We studied the association of infarct scar versus lipomatous metaplasia (LM) with the activation recovery interval (ARI) in putative ventricular tachycardia (VT) corridors traversing the infarct zone. Methods: The cohort included 32 patients from the prospective Intra-Myocardial Fat Deposition and Ventricular Tachycardia in Ischemic Cardiomyopathy (INFINITY) study. We defined myocardial scar, border zone (BZ) and potential viable corridors through infarct by late gadolinium enhancement (LGE)-cardiac magnetic resonance (CMR), and LM by computed tomography (CT). The images were registered with electroanatomic maps wherein the ARI of each point (1,530 within LM, 4,946 within scar) was calculated using a custom Python code as the time interval from the minimum derivative within the QRS to the maximum derivative within the T wave. ARI dispersion was defined as the standard deviation (SD) of ARI per AHA segment. Multilevel random effects linear regression models, clustered by patient, were used to evaluate the association between ARI (or ARI dispersion) with tissue types. Results: LM exhibited higher myocardial ARI than normal myocardium, BZ, scar [regression coefficient: 35.5 vs. 0, 11.4, and 25.4, P &lt;0.001]. Of 100 corridors computed from LGE-CMR and electrophysiologically confirmed to participate in VT reentry, 97 traversed through or near LM, and displayed prolonged ARI compared to 123 non-critical corridors distant from LM [356 (319, 396) vs. 283 (266, 316) ms, P &lt;0.001, Figure 1]. The association of LM with Log(ARI SD ) was more robust than that of scar (likelihood ratio χ 2 47.5 vs. 23.4, and 5.9% vs. 1.6% increase in Log(ARI SD ) /1 cm 2 increase per AHA segment, respectively). Additionally, LM and scar exhibited interaction (p&lt;0.001) in their association with Log(ARI SD ). Conclusion: LM is closely associated with prolonged local action potential duration of corridors and ARI dispersion, which may facilitate the propensity of VT circuit reentry.

Lipomatous Metaplasia Enables Ventricular Tachycardia by ReducingCurrent Loss Within theProtected Corridor.

Post-myocardial infarction ventricular tachycardia (VT) is due to re-entry through surviving conductive myocardial corridors across infarcted tissue. However, not all conductive corridors participate in re-entry. This study sought to test the hypothesis that critical VT corridors are more likely to traverse near lipomatous metaplasia (LM) and that current loss is reduced during impulse propagation through such corridors. Among 30 patients in the Prospective 2-center INFINITY (Intra-Myocardial Fat Deposition and Ventricular Tachycardia in Cardiomyopathy) study, potential VT-viable corridors within myocardial scar or LM were computed from late gadolinium enhancement cardiac magnetic resonance images. Because late gadolinium enhancement highlights both scar and LM, LM was distinguished from scar by using computed tomography. The SD of the current along each corridor was measured. Scar exhibited lower impedance than LM (median Z-score -0.22 [IQR: -0.84 to 0.35] vs -0.07 [IQR: -0.67 to 0.54]; P&lt; 0.001). Among all 381 corridors, 84 were proven to participate in VT re-entry circuits, 83 (99%) of which traversed or were adjacent to LM. In comparison, only 13 (4%) non-VT corridors were adjacent to LM. Critical corridors adjacent to LM displayed lower SD of current compared with noncritical corridors through scar but distant from LM (2.0[IQR: 1.0 to 3.4] μA vs 8.4 [IQR: 5.5 to 12.8] μA; P&lt; 0.001). Corridors critical to VT circuitry traverse infarcted tissue through or near LM. This association is likely mediated by increased regional resistance and reduced current loss as impulses traverse corridors adjacent to LM.

The Role of Epicardial Adipose Tissue in the Development of Atrial Fibrillation, Coronary Artery Disease and Chronic Heart Failure in the Context of Obesity and Type 2 Diabetes Mellitus: A Narrative Review

Cardiovascular diseases (CVDs) are a significant burden globally and are especially prevalent in obese and/or diabetic populations. Epicardial adipose tissue (EAT) surrounding the heart has been implicated in the development of CVDs as EAT can shift from a protective to a maladaptive phenotype in diseased states. In diabetic and obese patients, an elevated EAT mass both secretes pro-fibrotic/pro-inflammatory adipokines and forms intramyocardial fibrofatty infiltrates. This narrative review considers the proposed pathophysiological roles of EAT in CVDs. Diabetes is associated with a disordered energy utilization in the heart, which promotes intramyocardial fat and structural remodeling. Fibrofatty infiltrates are associated with abnormal cardiomyocyte calcium handling and repolarization, increasing the probability of afterdepolarizations. The inflammatory phenotype also promotes lateralization of connexin (Cx) proteins, undermining unidirectional conduction. These changes are associated with conduction heterogeneity, together creating a substrate for atrial fibrillation (AF). EAT is also strongly implicated in coronary artery disease (CAD); inflammatory adipokines from peri-vascular fat can modulate intra-luminal homeostasis through an “outside-to-inside” mechanism. EAT is also a significant source of sympathetic neurotransmitters, which promote progressive diastolic dysfunction with eventual cardiac failure. Further investigations on the behavior of EAT in diabetic/obese patients with CVD could help elucidate the pathogenesis and uncover potential therapeutic targets.

Association of left ventricular tissue heterogeneity and intramyocardial fat on computed tomography with ventricular arrhythmias in ischemic cardiomyopathy.

BackgroundGray zone, a measure of tissue heterogeneity on late gadolinium enhanced–cardiac magnetic resonance (LGE-CMR) imaging, has been shown to predict ventricular arrhythmias (VAs) in ischemic cardiomyopathy (ICM) patients. However, no studies have described whether left ventricular (LV) tissue heterogeneity and intramyocardial fat mass on contrast-enhanced computed tomography (CE-CT), which provides greater spatial resolution, is useful for assessing the risk of VAs in ICM patients with LV systolic dysfunction and no previous VAs.ObjectiveThe purpose of this proof-of-concept study was to determine the feasibility of measuring global LV tissue heterogeneity and intramyocardial fat mass by CE-CT for predicting the risk of VAs in ICM patients with LV systolic dysfunction and no previous history of VAs.MethodsPatients with left ventricular ejection fraction ≤35% and no previous VAs were enrolled in a prospective, observational registry and underwent LGE-CMR. From this cohort, patients with ICM who additionally received CE-CT were included in the present analysis. Gray zone on LGE-CMR was defined as myocardium with signal intensity (SI) > peak SI of healthy myocardium but <50% maximal SI. Tissue heterogeneity on CE-CT was defined as the standard deviation of the Hounsfield unit image gradients (HU/mm) within the myocardium. Intramyocardial fat on CE-CT was identified as regions of image pixels between –180 and –5 HU. The primary outcome was VAs, defined as appropriate implantable cardioverter-defibrillator shock or sudden arrhythmic death.ResultsThe study consisted of 47 ICM patients, 13 (27.7%) of whom experienced VA events during mean follow-up of 5.6 ± 3.4 years. Increasing tissue heterogeneity (per HU/mm) was significantly associated with VAs after multivariable adjustment, including for gray zone (odds ratio [OR] 1.22; P = .019). Consistently, patients with tissue heterogeneity values greater than or equal to the median (≥22.2 HU/mm) had >13-fold significantly increased risk of VA events, relative to patients with values lower than the median, after multivariable adjustment that included gray zone (OR 13.13; P = .028). The addition of tissue heterogeneity to gray zone improved prediction of VAs (area under receiver operating characteristic curve increased from 0.815 to 0.876). No association was found between intramyocardial fat mass on CE-CT and VAs (OR 1.00; P = .989).ConclusionIn ICM patients, CE-CT–derived LV tissue heterogeneity was independently associated with VAs and may represent a novel marker useful for risk stratification.

Strategies for Imaging Metabolic Remodeling of the Heart in Obesity and Heart Failure.

Define early myocardial metabolic changes among patients with obesity and heart failure, and to describe noninvasive methods and their applications for imaging cardiac metabolic remodeling. Metabolic remodeling precedes, triggers, and sustains functional and structural remodeling in the stressed heart. Alterations in cardiac metabolism can be assessed by using a variety of molecular probes. The glucose tracer analog, 18F-FDG, and the labeled tracer 11C-palmitate are still the most commonly used tracers to assess glucose and fatty acid metabolism, respectively. The development of new tracer analogs and imaging agents, including those targeting the peroxisome proliferator-activated receptor (PPAR), provides new opportunities for imaging metabolic activities at a molecular level. While the use of cardiac magnetic resonance spectroscopy in the clinical setting is limited to the assessment of intramyocardial and epicardial fat, new technical improvements are likely to increase its usage in the setting of heart failure. Noninvasive imaging methods are an effective tool for the serial assessment of alterations in cardiac metabolism, either during disease progression, or in response to treatment.

Substrate Modification Using Stereotactic Radioablation to Treat Refractory Ventricular Tachycardia in Patients With Ischemic Cardiomyopathy.

This study aimed to determine the feasibility of using radioablation for arrhythmogenic a substrate modification. Stereotactic body radiation therapy (SBRT) is a promising therapy for ventricular tachycardia (VT) refractory to catheter ablation. A total of 6 male patients (median age 72 years) with ischemic cardiomyopathy (left ventricular ejection fraction 20% [interquartile range (IQR): 16%-25%]) and VT refractory to antiarrhythmic medications and catheter ablations underwent SBRT to extensive scar substrate. In addition to electroanatomical mapping, 5 of 6 patients had computed tomography segmentation using MUSIC (IHU Liryc, Univ. Bordeaux and Inria Sophia Antipolis, France). Regions of wall thinning<5mm, calcification, and intramyocardial fat were targeted for radioablation at 25 Gy. The median planning target volume was 319 (IQR: 280-330) mL. Device-treated or sustained VT episodes were not significantly reduced by radioablation (median 42 [IQR: 19-269] to 29 [IQR: 0-81]; P=0.438). However, a reduction in device shocks was observed from 12 (IQR: 3-19) to 0 (IQR: 0-1) (P=0.046). Over a follow-up period of 231 (IQR: 212-311) days, 3 patients died of end-stage heart failure and 3 of 6 patients had possible adverse events (heart failure exacerbation, pneumonia, and an asymptomatic pericardial effusion). Substrate modification using SBRT assisted by computed tomography segmentation is feasible for treatment of VT in patients with ischemic cardiomyopathy. Although a significant reduction in device shocks was observed, suboptimal VT burden reduction and significant mortality rate in this cohort of patients with advanced cardiomyopathy underscore the need to improve mechanistic understanding for antiarrhythmic effects to guide dosing and targeting of scar substrates.

Longitudinal effect of myocardial fat deposition on left ventricular diastolic function: a retrospective cohort study.

There is a known correlation between myocardial steatosis and heart function, but it is unclear how left ventricular diastolic function worsens over time in the myocardial steatosis setting. We sought to investigate whether intramyocardial fat deposition affects diastolic function over time. This was a retrospective analysis of patients who had undergone 1-3 echocardiography assessments between April 2011 and April 2017. Patients were divided into two groups: those with the presence of myocardial fat deposition in the left ventricular myocardium (assessed by having tissue within any 10-mm2 region with computed tomography values between - 190 and - 30 Hounsfield units; + MF), and those with absence of deposition not meeting the threshold (- MF). The rates of change of the standard early diastolic mitral annulus velocity (e') and the transmitral early peak velocity (E)/e' ratio at the second and third echocardiograph assessments were calculated relative to baseline. In total, 125 patients were eligible (+ MF, n = 39; - MF, n = 86) for inclusion. Compared with the - MF group, e' was significantly lower and E/e' was significantly higher in the + MF group at each scan timepoint, even when adjusted for body mass index and sex. A significant average decrease in e' and increase in E/e' was also observed in the + MF group across all scans compared with the - MF group. Myocardial steatosis was associated with an acceleration of decreased left ventricular diastolic function over time.

Cardiothoracic imaging findings of Proteus syndrome

In this work, we sought to delineate the prevalence of cardiothoracic imaging findings of Proteus syndrome in a large cohort at our institution. Of 53 individuals with a confirmed diagnosis of Proteus syndrome at our institution from 10/2001 to 10/2019, 38 individuals (men, n = 23; average age = 24 years) underwent cardiothoracic imaging (routine chest CT, CT pulmonary angiography and/or cardiac MRI). All studies were retrospectively and independently reviewed by two fellowship-trained cardiothoracic readers. Disagreements were resolved by consensus. Differences between variables were analyzed via parametric and nonparametric tests based on the normality of the distribution. The cardiothoracic findings of Proteus syndrome were diverse, but several were much more common and included: scoliosis from bony overgrowth (94%), pulmonary venous dilation (62%), band-like areas of lung scarring (56%), and hyperlucent lung parenchyma (50%). In addition, of 20 individuals who underwent cardiac MRI, 9/20 (45%) had intramyocardial fat, mostly involving the endocardial surface of the left ventricular septal wall. There was no statistically significant difference among the functional cardiac parameters between individuals with and without intramyocardial fat. Only one individual with intramyocardial fat had mildly decreased function (LVEF = 53%), while all others had normal ejection fraction.

Prognostic Role of Left Ventricular Intramyocardial Fatty Metaplasia in Patients With Previous Myocarditis (MYOFAT Study)

Left ventricular intramyocardial fat (LV-IMF) is often found in patients with previous irreversible myocardial damage and may be detected by cardiac magnetic resonance (CMR). No data are currently available about the prevalence of LV-IMF in patients with previous myocarditis. Our aim was to assess the prevalence of LV-IMF in patients with previous myocarditis by repeating after >3 years a follow-up CMR examination and to evaluate its clinical and prognostic role. Patients with clinical suspected myocarditis who underwent CMR within the first week from the onset of their symptoms and underwent repeated CMR were enrolled. LV-IMF was detected as areas of left ventricular intramyocardial "India ink" black boundary with or without a hyperintense core. Overall, in 235 patients with a definitive diagnosis of acute myocarditis, CMR was repeated after a median of 4 (3 to 6) years from symptom onset. LV-IMF positive patients (n = 35, 15%) presented greater ventricular volumes and more frequently a mid-wall late gadolinium enhancement than those without LV-IMF (both p < 0.05). Patients presenting major cardiac events (sudden cardiac deaths, resuscitated cardiac arrest, and appropriate implantable cardioverter-defibrillator-firing) at follow-up had a greater prevalence of LV-IMF than those without (55% vs 11%, p < 0.001). Patients with LV-IMF had a higher incidence myocarditis relapse (27% vs 9%, p = 0.003) and a greater risk of major cardiac events (p < 0.0001) than those without. At logistic regression analysis, LV-IMF was an independent predictor of major cardiac events. In conclusion, LV-IMF is not an uncommon finding in patients with previous myocarditis and is associated with worse ventricular remodeling and prognosis.