Ischemic Cardiomyopathy Research Articles

Magnetocardiography in the Evaluation of Sudden Cardiac Death Risk: A Systematic Review.

Sudden cardiac death (SCD) is responsible for 15%-20% of deaths globally/year, predominantly due to ventricular arrhythmias (VA) caused by vulnerable cardiac substrate. Identifying those at risk has proved difficult with several limitations of current methods. We evaluated the evidence for magnetocardiography (MCG) in predicting SCD events. We searched Embase/Medline databases for English language papers evaluating MCG in patients at risk of VA. A total of 119 papers were screened with 27 papers included for analysis (23 case-controlled, four cohort studies); study sizes varied (n = 12 to 158). Etiology was ischemic cardiomyopathy (ICM) in 22, dilated cardiomyopathy in 2, arrhythmogenic cardiomyopathy in 1 and mixed in 2. In patients with ICM there were consistent discriminatory features seen using time-based and signal-complexity measures that persisted when evaluating the independence of these parameters. Current flow analysis demonstrated promising discriminatory results in other etiologies. The features studied support the role of MCG in identifying substrate for VA, particularly in ICM.

Frailty, age, and treatment effect of surgical coronary revascularization in ischemic cardiomyopathy: a post hoc analysis of the STICHES trial.

Frailty is common among older patients with heart failure (HF). The efficacy of coronary artery bypass grafting (CABG) on the risk of mortality amongfrailpatients with ischemic cardiomyopathy and HF is uncertain, and whether frailty burden modifies the treatment benefits of CABG among these patients is unknown. We performed a post hoc analysis of the STICHES trial, a randomized trial of CABG with medical therapy vs medical therapy alone among participants with ischemic cardiomyopathy with ejection fraction ≤ 35%. Baseline frailty was assessed through a Rockwood Frailty Index (FI), and based on FI cut-offs from prior HF studies, participants with FI ≥ 0.311 were classified as more frail, and those with FI < 0.311 were classified as less frail. A multivariable Cox proportional hazard model with multiplicative interaction terms was constructed to evaluate whether frailty status modified the treatment effect of CABG on mortalityin the overall trial cohort and among those < 60 vs ≥ 60 years of age. Of 1187 participants (12.4% female, 2.6% Black, median FI = 0.33 [IQR 0.27-0.39]), 678 were characterized as more frail. Frailty burden did not modify the efficacy of CABG on the risk of all-cause death in the overall cohort (Pint CABG × frailty = 0.2). In age stratified analysis,Baseline frailty status did not modify the treatment effect of CABG on the risk of all-cause mortality among younger (< 60years, Pint CABG × frailty = 0.2) as well as older participants (≥60years, Pint CABG × frailty = 0.6). In this post hoc analysis of the STICHES trial, baseline frailty status did not modify the efficacy of CABG in the overall cohort as well asamong younger or older participants. Frailty alone should not be used as a criterion to determine the utilization of CABG among patients with ischemic cardiomyopathy.

Uncovering underlying cause for heart failure in a 51-year-old woman with fibromuscular dysplasia

Abstract Introduction/Objective Arrhythmogenic cardiomyopathy is a rare disorder characterized by the replacement of the myocardium with fibroadipose tissue, usually affecting the right ventricle and rarely affecting the left. Methods/Case Report We present the case of a 51-year-old woman with past medical history including fibromuscular dysplasia of the internal carotid arteries and suspected ischemic cardiomyopathy with reduced ejection fraction awaiting heart transplant. The patient suffered a spontaneous coronary artery dissection eight years prior, which was the inciting factor that led to the decline in her cardiac function. After transplant, gross examination of the explanted heart showed a moderate amount of epicardial fat and visible intramural ventricular adipose tissue deposits in the myocardium. On histology, both the right and left ventricle walls showed extensive microscopic fatty infiltration along with focal involvement of the interventricular septum. These findings supported the final diagnosis of arrhythmogenic cardiomyopathy of the right and left ventricle, as well as involvement of the interventricular septum making this case especially rare. There were no signs of infarct or ischemic damage, contrary to what was expected given her diagnosis of ischemic cardiomyopathy. Results (if a Case Study enter NA) NA Conclusion The pathological work-up of this case shed light on the true nature of the patient’s cardiomyopathy and has prompted further genetic testing, as arrhythmogenic cardiomyopathy can be caused by several different genetic mutations. In addition to this work-up, a thorough literature review was performed looking for connections between arrhythmogenic cardiomyopathy and fibromuscular dysplasia, as arrhythmogenic cardiomyopathy is not often seen in this setting. Although no direct connection between the two was uncovered, it was found in the literature that a polymorphism in the Phosphatase and Actin Regulator 1 (PHACTR1) gene has been identified as a genetic component of fibromuscular dysplasia. This variant has been linked to spontaneous coronary artery dissection, which our patient experienced at the young age of 43. This could prompt further genetic investigation into her fibromuscular dysplasia in addition to the genetic work up already being done for her arrhythmogenic cardiomyopathy. This case highlights how rare etiologies can be uncovered through diligent histological analysis, and how further analysis using laboratory techniques such as genetic testing can help patients understand the full breadth of their conditions.

Ten hour donor heart ischemic time with 10ºC static storage

Utilization of 10ºC static storage safely extended both ischemic time and travel radius in heart transplantation. A 57-year-old man with ischemic cardiomyopathy, a left ventricular assist device (LVAD), and end-stage renal disease was listed for combined heart-kidney transplant. The donor hospital in Anchorage, AK, was located approximately 2,700 nautical miles and 8 hours from the recipient center. The organ was transported in 10ºC static storage with over 10 hours of ischemic time and had superb early allograft function. Excellent outcomes with extended ischemic times can be achieved without machine perfusion, provided good recovery, storage, and implant techniques are followed.

Comparison of Electrocardiogram between Dilated Cardiomyopathy and Ischemic Cardiomyopathy Based on Empirical Mode Decomposition and Variational Mode Decomposition.

The clinical manifestations of ischemic cardiomyopathy (ICM) bear resemblance to dilated cardiomyopathy (DCM), yet their treatments and prognoses are quite different. Early differentiation between these conditions yields positive outcomes, but the gold standard (coronary angiography) is invasive. The potential use of ECG signals based on variational mode decomposition (VMD) as an alternative remains underexplored. An ECG dataset containing 87 subjects (44 DCM, 43 ICM) is pre-processed for denoising and heartbeat division. Firstly, the ECG signal is processed by empirical mode decomposition (EMD) and VMD. And then, five modes are determined by correlation analysis. Secondly, bispectral analysis is conducted on these modes, extracting corresponding bispectral and nonlinear features. Finally, the features are processed using five machine learning classification models, and a comparative assessment of their classification efficacy is facilitated. The results show that the technique proposed provides a better categorization for DCM and ICM using ECG signals compared to previous approaches, with a highest classification accuracy of 98.30%. Moreover, VMD consistently outperforms EMD under diverse conditions such as different modes, leads, and classifiers. The superiority of VMD on ECG analysis is verified.

Ablation options for sub-epicardially located ventricular substrates responsible for ventricular tachycardia: where is it all headed?

Patients with nonischemic and ischemic cardiomyopathy (NICM and ICM) exhibit re-entrant tachycardias related to scar tissue in subepicardial, in addition to typical subendocardial locations. Control of ventricular arrhythmias related to these targets has remained elusive despite advances in mapping and ablation technology. Percutaneous epicardial ablation is the standard after failed endocardial ventricular ablation, but recurrence rates are disappointing. Pulsed-field energy has been associated with coronary artery spasm and therefore may be less suitable for epicardial ablation. Commercially available energy sources, including pulsed-field, have limited depths of myocardial penetration when applied epicardially. Lateral volumetric thermal spreading of ablation injury is associated with decreasing depth of ablation and is difficult to control. A new cryoablation technology based on liquid helium and developed specifically for epicardial work may be able to overcome these limitations. Ablation strategies that can improve lesion formation in subepicardial ventricular myocardium may improve outcomes of ablation in nonsubendocardial NICM and ICM targets.

Cardiac Resynchronization Therapy in Ischemic Versus Nonischemic Cardiomyopathy: Patient-Level Meta-Analysis of 7 Randomized Clinical Trials

BackgroundData on whether cardiac resynchronization therapy (CRT) results in better clinical and echocardiographic outcomes in patients with nonischemic cardiomyopathy (NICM) vs ischemic cardiomyopathy (ICM) are conflicting. ObjectivesThe authors conducted this meta-analysis of 7 clinical trials of CRT to determine the association between etiology of cardiomyopathy and clinical and echocardiographic outcomes. MethodsThe authors analyzed patient-level data using Bayesian Hierarchical Weibull survival regression modeling to determine the association between etiology of cardiomyopathy and time to all-cause death or heart failure hospitalization (HFH). Linear regression was used to assess the association between etiology of cardiomyopathy and echocardiographic measurements. ResultsOf 6,252 patients included, 4,717 (75%) were men, median age was 66 years (IQR: 58-73 years), 3,704 (59%) had ICM, and 3,778 (60%) received CRT. CRT increased the time to HFH or all-cause death (HR: 0.67; 95% credible interval [CrI]: 0.56-0.82; P < 0.001) with no difference by etiology of cardiomyopathy (HR ratio: 1.06 [95% CrI: 0.87-1.29]; P = 0.57). Likewise, CRT increased the time to all-cause death (HR: 0.71 [95% CrI: 0.55-0.93]; P = 0.019) with no difference by etiology of cardiomyopathy (HR ratio: 1.06 [95% CrI: 0.80-1.43]; P = 0.70). Echocardiographic data that were available for 2,430 (39%) patients showed that CRT improvements in left ventricular ejection fraction, left ventricular end-diastolic diameter, and left ventricular end-systolic diameter were larger for patients with NICM. ConclusionsAlthough CRT led to greater increases in left ventricular ejection fraction and reductions in ventricular dimensions for patients with NICM compared with those with ICM, CRT significantly increased the time to HFH or all-cause death independently of the etiology of cardiomyopathy. Further studies on improving patient selection for CRT are needed.

Injury-induced myosin-specific tissue-resident memory T cells drive immune checkpoint inhibitor myocarditis

Cardiac myosin-specific (MyHC) T cells drive the disease pathogenesis of immune checkpoint inhibitor-associated myocarditis (ICI-myocarditis). To determine whether MyHC T cells are tissue-resident memory T (TRM) cells, we characterized cardiac TRM cells in naive mice and established that they have a distinct phenotypic and transcriptional profile that can be defined by their upregulation of CD69, PD-1, and CXCR6. We then investigated the effects of cardiac injury through a modified experimental autoimmune myocarditis mouse model and an ischemia-reperfusion injury mouse model and determined that cardiac inflammation induces the recruitment of autoreactive MyHC TRM cells, which coexpress PD-1 and CD69. To investigate whether the recruited MyHC TRM cells could increase susceptibility to ICI-myocarditis, we developed a two-hit ICI-myocarditis mouse model where cardiac injury was induced, mice were allowed to recover, and then were treated with anti-PD-1 antibodies. We determined that mice who recover from cardiac injury are more susceptible to ICI-myocarditis development. We found that murine and human TRM cells share a similar location in the heart and aggregate along the perimyocardium. We phenotyped cells obtained from pericardial fluid from patients diagnosed with dilated cardiomyopathy and ischemic cardiomyopathy and established that pericardial T cells are predominantly CD69+ TRM cells that up-regulate PD-1. Finally, we determined that human pericardial macrophages produce IL-15, which supports and maintains pericardial TRM cells.

Gene expression profiles, potential targets and treatments of cardiac remodeling.

Hypertensive and ischemic heart diseases have high morbidity all over the world, and they primarily contribute to heart failure associated with high mortality. Cardiac remodeling, as a basic pathological process in heart diseases, is mainly comprised of cardiac hypertrophy and fibrosis, as well as cell death which occurs especially in the ischemic cardiomyopathy. Myocardial remodeling has been widely investigated by a variety of animal models, including pressure overload, angiotensin II stimulation, and myocardial infarction. Pressure overload can cause compensatory cardiac hypertrophy at the early stage, followed by decompensatory hypertrophy and heart failure at the end. Recently, RNA sequencing and differentially expressed gene (DEG) analyses have been extensively employed to elucidate the molecular mechanisms of cardiac remodeling and related heart failure, which also provide potential targets for high-throughput drug screenings. In this review, we summarize recent advancements in gene expression profiling, related gene functions, and signaling pathways pertinent to myocardial remodeling induced by pressure overload at distinct stages, ischemia-reperfusion, myocardial infarction, and diabetes. We also discuss the effects of sex differences and inflammation on DEGs and their transcriptional regulatory mechanisms in cardiac remodeling. Additionally, we summarize emerging therapeutic agents and strategies aimed at modulating gene expression profiles during myocardial remodeling.

Essential Role of the RIα Subunit of cAMP-Dependent Protein Kinase in Regulating Cardiac Contractility and Heart Failure Development.

The heart expresses 2 main subtypes of cAMP-dependent protein kinase (PKA; type I and II) that differ in their regulatory subunits, RIα and RIIα. Embryonic lethality of RIα knockout mice limits the current understanding of type I PKA function in the myocardium. The objective of this study was to test the role of RIα in adult heart contractility and pathological remodeling. We measured PKA subunit expression in human heart and developed a conditional mouse model with cardiomyocyte-specific knockout of RIα (RIα-icKO). Myocardial structure and function were evaluated by echocardiography, histology, and ECG and in Langendorff-perfused hearts. PKA activity and cAMP levels were determined by immunoassay, and phosphorylation of PKA targets was assessed by Western blot. L-type Ca2+ current (ICa,L), sarcomere shortening, Ca2+ transients, Ca2+ sparks and waves, and subcellular cAMP were recorded in isolated ventricular myocytes (VMs). RIα protein was decreased by 50% in failing human heart with ischemic cardiomyopathy and by 75% in the ventricles and in VMs from RIα-icKO mice but not in atria or sinoatrial node. Basal PKA activity was increased ≈3-fold in RIα-icKO VMs. In young RIα-icKO mice, left ventricular ejection fraction was increased and the negative inotropic effect of propranolol was prevented, whereas heart rate and the negative chronotropic effect of propranolol were not modified. Phosphorylation of phospholamban, ryanodine receptor, troponin I, and cardiac myosin-binding protein C at PKA sites was increased in propranolol-treated RIα-icKO mice. Hearts from RIα-icKO mice were hypercontractile, associated with increased ICa,L, and [Ca2+]i transients and sarcomere shortening in VMs. These effects were suppressed by the PKA inhibitor, H89. Global cAMP content was decreased in RIα-icKO hearts, whereas local cAMP at the phospholamban/sarcoplasmic reticulum Ca2+ ATPase complex was unchanged in RIα-icKO VMs. RIα-icKO VMs had an increased frequency of Ca2+ sparks and proarrhythmic Ca2+ waves, and RIα-icKO mice had an increased susceptibility to ventricular tachycardia. On aging, RIα-icKO mice showed progressive contractile dysfunction, cardiac hypertrophy, and fibrosis, culminating in congestive heart failure with reduced ejection fraction that caused 50% mortality at 1 year. These results identify RIα as a key negative regulator of cardiac contractile function, arrhythmia, and pathological remodeling.

TCT-792 Prognosis in Patients With Cardiogenic Shock According to Sex, With or Without Ischemic Cardiomyopathy

TCT-792 Prognosis in Patients With Cardiogenic Shock According to Sex, With or Without Ischemic Cardiomyopathy

Revascularization in ischemic cardiomyopathy. Is viability testing still viable?

Revascularization in ischemic cardiomyopathy. Is viability testing still viable?

Emergent Ablation for VentricularTachycardia: Predictors of Prolonged Hospitalization and Mortality.

Patients with ventricular tachycardia (VT) frequently present in unstable VT and are subject to urgent/high-risk ablation procedures. Clinical predictors of prolonged hospitalization and mortality are needed for optimal management of these patients. This study seeks to identify factors associated with prolonged hospitalization and mortality in emergent unplanned VT ablation procedures. Fifty consecutive patients hospitalized emergently for VT with structural heart disease who underwent catheter ablation were prospectively followed up for outcomes and complications. Of the 50 patients (mean ± SD age 67.6 ± 12.8 years), 86.0% were male, 62.0% had ischemic cardiomyopathy, and their median left ventricular ejection fraction was 28.5%. Hospital stay<7days (median 3days) occurred in 28 (56.0%) patients (Group 1) and >7days (median 10days) or death<7days occurred in 22 (44.0%) patients (Group 2). PAINESD score and left ventricular ejection fraction were similar between the groups. Compared with Group 1, Group 2 had significantly worse NYHA functional class III or higher (25.0% vs 63.6%; P=0.006), electrical storm (46.4% vs 77.3%; P=0.027), and prior failed VT ablation (35.7% vs 68.2%; P=0.023). Multivariable analysis showed that NYHA functional class III or higher and prior failed VT ablation were predictive of prolonged hospital stay. After ablation, compared with Group 1, Group 2 had worse heart failure (10.7% vs 54.5%; P=0.001), VT recurrences (3.6% vs 68.2%; P< 0.001), and 7 deaths within 30days. Patients undergoing emergent VT ablation are at high risk for prolonged hospital stay, which is predicted by NYHA functional class III or higher and a prior failed ablation. Early VT recurrences and worsening heart failure contribute to prolonged hospitalization and a high 30-day mortality.

Secondary mitral regurgitation surgical management: a narrative review.

The most common valvular heart disease in the US is moderate to severe mitral regurgitation (MR). Function MR or secondary MR comprises many of these cases. Moderate and severe secondary MR are independently associated with increased all-cause mortality and rehospitalization for heart failure. Both ischemic and nonischemic cardiomyopathy can cause secondary MR via similar pathophysiology that leads to inadequate valve leaflets coaptation. The management of secondary MR is complex. The optimal treatment strategy for secondary MR remains controversial, reflected in the vast array of treatment options and the complexity of therapeutic decision-making. Several surgical mitral valve repair techniques have been described in the literature. Many of these aims to facilitate adequate valve leaflet coaptation. In this review, the pathophysiology of MR is described with a focus on evaluating and managing secondary MR. A literature review was performed using PubMed and Google Scholar. Clinical trials, meta-analyses, randomized controlled trials, reviews, and systematic reviews were considered from January 1, 1995 through December 31, 2022. Articles published in languages other than English with limited text availability were excluded. Optimal therapeutic approach in severe secondary MR is complex and several patient factor should be considered. We provide a framework for the surgical management of secondary MR based on echocardiographic parameters, the presence of ischemia, and myocardial viability. Further study is needed to guide the selection of patients most likely to benefit from mitral valve repair or replacement in the setting of secondary MR.

TCT-254 Importance of Change in LVEF with PCI on Risk of Cardiac Death or Hospitalization for Heart Failure in Patients With Stable Ischemic Cardiomyopathy

TCT-254 Importance of Change in LVEF with PCI on Risk of Cardiac Death or Hospitalization for Heart Failure in Patients With Stable Ischemic Cardiomyopathy

Cardiac Resynchronization Therapy with Defibrillator in Ischemic Versus Nonischemic Cardiomyopathy.

Cardiac resynchronization therapy with implantable cardioverter defibrillators (CRT-Ds) are established therapy options for patients suffering from heart failure (HF). Several aspects of HF modification have yet to be described regarding etiology-dependent outcome differences in the long-term.The Mannheim CArdiac Resynchronization TherApy RetrospeCtive ObservAtioNAl (MARACANA) Registry retrospectively included all patients provided with CRTs in our center from 2013 to 2021. CRT-D recipients (n = 380) were grouped to either ischemic cardiomyopathy (ICM, n = 206) or nonischemic cardiomyopathy (NICM, n = 174). Both groups were compared regarding survival, left ventricular ejection fraction (LVEF), hospitalizations due to HF, intrinsic and paced QRS width, NYHA classification, and several further aspects of HF modification in the long-term (59.1 ± 4.81 months).Patients with ICM were older (73.3 ± 8.4 versus 67.7 ± 10.8 years) and predominantly male (86.4 versus 74.7%) and presented with higher creatinine values (1.57 ± 0.92 versus 1.31 ± 0.66 mg/dL, each P < 0.05) at baseline. The mean survival for patients with NICM was better (51.9 ± 1.2 versus 54.4 ± 1.1 months, P = 0.03). Improvements in NYHA (2.93 ± 0.4 versus 2.79 ± 0.5-2.19 ± 0.7 versus 1.79 ± 0.7) and LVEF (26.4 ± 6.8 versus 27% ± 6.9% to 35.7 ± 9.6 versus 44 ± 11%, each P < 0.05) were similar for both groups after 5 years. Patients with ICM experienced more hospitalizations due to HF within the first year (odds ratio 1.9, P < 0.05), whereas electrical remodeling was more impressive for NICM (QRS width 157.1 ± 19.4 milliseconds versus intrinsic 116.6 ± 12.7 milliseconds and paced 131.9 ± 21 milliseconds after 5 years, both P < 0.05).Patients with HF might experience long-term improvements in functional status and left ventricular reverse remodeling following CRT-D, regardless of underlying etiology. Alterations in some aspects of HF modification could be influenced by time- and etiology-associated comorbidities.

3D-targeted, electrocardiographic imaging-aided stereotactic radioablation for ventricular tachycardia storm: a case report

Abstract Background Stereotactic arrhythmia radioablation (STAR) is a promising non-invasive therapy for patients with ventricular tachycardia (VT). Accurate identification of the arrhythmogenic volume, or clinical target volume (CTV), on the radiotherapy (RT) 4D planning computed tomography (CT) scan is key for STAR efficacy and safety. This case report illustrates our workflow of electro-structural image integration for CTV delineation. Case summary A 72-year-old man with ischaemic cardiomyopathy and VT storm, despite two (endocardial and epicardial) catheter-based ablations, was consented for STAR. A 3D electro-structural arrhythmia model was generated from co-registered electroanatomical voltage and activation maps, electrocardiographic (ECG) imaging, and the cardiac CT angiography scan (in ADAS 3D), pinpointing the VT isthmus and inferoapical VT exit. At this location, an area with short recovery times was found with ECG imaging. A multidisciplinary team delineated the CTV on the transmural ventricular myocardium, which was fused with the 4D planning CT scan using a digital images and communication in medicine (DICOM) radiotherapy file. The CTV was 63% smaller compared with using the conventional American Heart Association 17-segment approach (11 vs. 24 cm3). A single fraction of 25 Gy was delivered to the internal target volume. After an 8-week blanking period, no VT recurrences or radiation-related side-effects were noted. Eight months later, the patient died from end-stage heart failure. Discussion We report a novel workflow for 3D-targeted and ECG imaging-aided CTV delineation for STAR, resulting in a smaller irradiated volume compared with segmental approaches. Acute and intermediate outcome and safety were favourable. Non-invasive ECG imaging at baseline and during induced VT holds promise for STAR guidance.

Is LVH a must in an amyloid heart?

Abstract Background Transthyretin amyloidosis (ATTR), an infiltrative cardiomyopathy, is characterized by the infiltration of transthyretin-derived amyloid fibrils into the cardiac extracellular space, which causes morphological and functional heart damage. Because of the vast range of symptoms that can accompany ATTR cardiac amyloidosis, the illness remains unknown. However, misdiagnosis or delayed diagnosis due to inconsistencies between clinical findings and the severity of the underlying disease hampers treatment methods. Aim and objectives This article investigates the intricate relationship between ATTR amyloidosis pathogenesis and clinical signs to understand better the challenges and advancements in early discovery, treatment, and prognosis of this concealed sickness. Methods &amp; Results Between November 2022 and April 2024, we conducted a prospective analysis on a cohort of 71 patients diagnosed with ATTR cardiac amyloidosis utilizing PYP imaging at our institution (Al Hada Armed Force Hospital, Taif, Saudi Arabia). The Medical Ethics Review Committee of the hospital accepted this project (2023-720). During our study, we faced two cases without LVH and both cases have grade II-III cardiac uptake. 1st case A 66-year-old male patient who is a known case of ischemic cardiomyopathy with EF 35% since 2018, he underwent PCI in 2018. The patient is following the cardio clinic since 2018 and on every visit he was asymptomatic, The Patient in 2021 experienced new shortness of breath within six minutes’ walk distance less than 400 meters. The patient experienced erectile dysfunction and underwent intervention for his carpal tunnel syndrome. ECG showed old Q in anterior leads. Echo showed the same EF 35% and old wall motion abnormalities. Diagnostic coronary angiography showed patent stents and no residual ischemia. When we revised his old echo study that was done in 2017, we found EF 55%, concentric LVH. PYP bone scintigraphy was decided and showed grade II-III cardiac uptake. 2nd case A 53-year-old hypothyroid female patient and she has metastatic left breast cancer. During her workup bone scan, grade III cardiac uptake was accidentally discovered using an HMDP isotope. The patient was referred to the cardio clinic where the patient denied any cardiac or non-cardiac symptoms. All her labs, ECG and Echo were within normal range. CMR showed diffuse subendocardial LGE suggestive of infiltrative disease. Conclusion Based on unique pathological features of CA that would present as morphological LVH with /without ECG evidence of LVH. We hypothesized that LVH would occur in the later stages of the disease or may be decreased due to other pathology as coronary artery disease. Clinical suspicion remains the cornerstone for early diagnosis and workup.

In-Hospital Outcomes of Ventricular Tachycardia Catheter Ablation in the Presence of Intra-Cardiac Thrombus.

Ventricular tachycardia (VT) catheter ablation in the presence of intracardiac thrombi was evaluated in very few studies. To investigate in-hospital outcomes of VT ablation in the presence of an intracardiac thrombus, in a large inpatient US registry. Using the National Inpatient Sample (NIS) database, patients who underwent non-elective VT catheter ablations in the United States between 2016 and 2019 were identified using ICD-10 codes. Sociodemographic, clinical data, in-hospital procedures, and outcomes as well as in-hospital mortality were collected. In-hospital outcomes were compared using propensity score (PS) matching analysis with a 1:3 ratio between patients with and without intracardiac thrombus. A weighted total of 15,725 admissions for non-elective VT ablation were included in the study, of which 190 (1.2%) had a discharge diagnosis of intracardiac thrombus. Patients with intracardiac thrombus had a higher comorbidity burden and were more likely to have ischemic cardiomyopathy and a diagnosis of cardiac aneurysm. In PS analysis, the presence of intracardiac thrombus was significantly associated with higher rates of any in-hospital complications (42.1%vs. 19.3%, p<0.009), driven by higher periprocedural cerebrovascular accident and vascular injury events. In-hospital mortality rates were not significantly different between the groups. In patients undergoing non-elective VT ablation, intracardiac thrombus was associated with higher rates of in-hospital complications, but not higher in-hospital mortality. These findings suggest that intracardiac thrombus should not contraindicate VT ablation when deemed necessary, while efforts should be made to decrease potential complications.

Immunomodulatory Therapy for Ischemic Heart Disease.

Ischemic heart disease is a leading cause of death worldwide, manifested clinically as myocardial infarction (and ischemic cardiomyopathy. Presently, there exists a notable scarcity of efficient interventions to restore cardiac function after myocardial infarction. Cumulative evidence suggests that impaired tissue immunity within the ischemic microenvironment aggravates cardiac dysfunction, contributing to progressive heart failure. Recent research breakthroughs propose immunotherapy as a potential approach by leveraging immune and stroma cells to recalibrate the immune microenvironment, holding significant promise for the treatment of ischemic heart disease. In this Primer, we highlight three emerging strategies for immunomodulatory therapy in managing ischemic cardiomyopathy: targeting vascular endothelial cells to rewire tissue immunity, reprogramming myeloid cells to bolster their reparative function, and utilizing adoptive T cell therapy to ameliorate fibrosis. We anticipate that immunomodulatory therapy will offer exciting opportunities for ischemic heart disease treatment.