Despite advances in our understanding of myocardial recovery among left ventricular assist device (LVAD) patients, with 10-30% of patients achieving substantial myocardial improvement, the rates of LVAD support cessation remain extremely low (1-2%). These numbers are in stark contrast to clinical trial data where successful LVAD cessation is reported in up to 47% of patients. The majority of LVAD programs lack structured recovery programs and targeted protocols, likely underscoring the heterogeneity that exists among LVAD patients with myocardial recovery. This perspective summarizes the current medical and surgical challenges with respect to 1) identifying the appropriate candidates for LVAD cessation; 2) methods to wean LVAD support; 3) reviewing surgical techniques for cessation of current generation HeartMate 3 LVAD; and 4) approaching shared decision making for LVAD cessation between patients and providers given the uncertainties that remain in the field.

Purpose The ice cooler method is the traditional method used to preserve and transport donors' hearts. The Paragonix SherpaPak Cardiac Transport System provides uniform cooling with temperatures from 4 to 8°C. In this study we aim to assess the clinical outcomes associated with these two methods at a large transplant center. Methods A retrospective review of consecutive adult heart transplant (HT) patients between 1/2021 to 6/2022. Patients were stratified by type of transportation method (Ice cooler vs. SherpaPak). Patient characteristics and post-transplant outcomes in HT recipients were analyzed using chi-square and Fisher tests. Results 100 patients were included in study, 40 transported with Ice cooler and 60 transported with SherpaPak. Patient age, gender and frequency of multi-organ transplants were identical between the groups (p=0.67, p=0.72 and p=0.84 respectively) . Patients in the SherpaPak group had a numerically shorter intensive care unit length of stay (6.5 days vs. 7.5 days). Severe primary graft dysfunction was also numerically less frequent in the SherpaPak group (8% versus 18% p=0.167). 90-day mortality was 5% in the ice cooler group and 3.3% in the SherpaPak group (p=ns). (Table) Conclusion SherpaPak Cardiac Transport System demonstrated favorable trends in short-term outcomes compared to the ice cooler transport method.

Introduction Performing heart transplantation (HT) in highly sensitized patients remains challenging from an immunological perspective, particularly in regard to post-HT surveillance and management. Donor-derived cell-free DNA (dd-cfDNA) is a non-invasive marker of graft injury and may be useful for monitoring highly sensitized patients Case Report A 71 year old woman presented with giant cell myocarditis and cardiogenic shock requiring HT. The patient was highly sensitized pre-transplant (cPRA = 100%) and underwent HT with a positive flow cytometry crossmatch (negative CDC crossmatch). Post-HT surveillance with routine EMB and dd-cfDNA levels was done per protocol. The patient was treated with tacrolimus, MMF and monthly Belatacept in addition to a steroid taper. Starting at 7 months post-HT, her dd-cfDNA levels were persistently elevated above baseline. She had no rejection on biopsy, normal graft function and low-level HLA class II donor-specific antibodies (DSA) . Due to elevated biomarkers and presence of DSA, she was treated with IVIG and Rituximab. At 1 year post-HT, she had 2R/3A rejection with reduced graft function in the setting of low Tacrolimus levels and was treated with pulse steroids. Following this episode, the ddcfDNA and troponin levels remained persistently elevated. Her biopsies were negative for rejection, and she was asymptomatic. DSA became negative. Cardiac MRI revealed mildly reduced graft function (LVEF =44%), no evident myocardial edema on T2 weighted imaging, and mildly reduced RV function. She had no detectable DSA. Given persistent troponin elevation with high dd-cfDNA levels (2.7%), she was again treated for chronic AMR with Rituximab and IVIG. Immediately after treatment initiation, her dd-cfDNA levels steadily declined Summary Management of highly sensitized patients following HT is complex and requires incorporation of multiple pieces of data to direct treatment. dd-cfDNA may provide crucial data for the detection of ongoing graft injury in these patients

A 67-year-old man with medical history of ischemic cardiomyopathy with stage D heart failure and infrarenal abdominal aortic aneurysm underwent implantation of a left ventricular assist device (LVAD). Three months after the procedure, he presented with unrelenting back pain and a rapidly increased in size aneurysm. The patient underwent urgent endovascular aneurysm repair with uncomplicated recovery. Growing experience with current-generation LVADs led to the recognition of a novel type of vasculopathy: LVAD-induced aortopathy and a preexisting aortopathy may rapidly progress after LVAD placement.

Heart failure (HF) is characterized by global alterations in myocardial DNA methylation, yet little is known about the epigenetic regulation of the noncoding genome and potential reversibility of DNA methylation with left ventricular assist device (LVAD) therapy. Genome-wide mapping of myocardial DNA methylation in 36 patients with HF at LVAD implantation, 8 patients at LVAD explantation, and 7 nonfailing (NF) donors using a high-density bead array platform identified 2,079 differentially methylated positions (DMPs) in ischemic cardiomyopathy (ICM) and 261 DMPs in nonischemic cardiomyopathy (NICM). LVAD support resulted in normalization of 3.2% of HF-associated DMPs. Methylation-expression correlation analysis yielded several protein-coding genes that are hypomethylated and upregulated (HTRA1, FBXO16, EFCAB13, and AKAP13) or hypermethylated and downregulated (TBX3) in HF. A potentially novel cardiac-specific super-enhancer long noncoding RNA (lncRNA) (LINC00881) is hypermethylated and downregulated in human HF. LINC00881 is an upstream regulator of sarcomere and calcium channel gene expression including MYH6, CACNA1C, and RYR2. LINC00881 knockdown reduces peak calcium amplitude in the beating human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs). These data suggest that HF-associated changes in myocardial DNA methylation within coding and noncoding genomes are minimally reversible with mechanical unloading. Epigenetic reprogramming strategies may be necessary to achieve sustained clinical recovery from heart failure.

AbstractBackgroundHuman heart failure is characterized by global alterations in the myocardial DNA methylation profile, yet little is known about epigenetic regulation of non-coding transcripts and potential reversibility of DNA methylation with left ventricular assist device (LVAD) support.MethodGenome-wide mapping of myocardial DNA methylation was performed in 36 patients with end-stage heart failure at the time of LVAD implant, 8 patients at the time of LVAD explant, and 7 non-failing controls using high-density bead array platform. Transcriptomic and functional studies were performed in human induced pluripotent stem cell derived cardiomyocytes (iPSCs).ResultsEtiology-specific analysis revealed 2079 differentially methylated positions (DMPs) in ischemic cardiomyopathy (ICM) and 261 DMPs in non-ischemic cardiomyopathy (NICM). 192 DMPs were common to ICM and NICM. Analysis of paired samples before and after LVAD support demonstrated reverse methylation of only 3.2% of HF-specific DMPs. Methylation-expression correlation analysis yielded several protein-coding genes that are hypomethylated and upregulated (HTRA1, FAM65A, FBXO16, EFCAB13, AKAP13, RPTOR) or hypermethylated and downregulated (TBX3) in ICM and NICM patients. A novel cardiac-specific super-enhancer lncRNA (LINC00881) is hypermethylated and downregulated in the failing human heart.LINC00881is an upstream regulator of sarcomere and calcium channel gene expression includingMYH6, CACNA1C, andRYR2. LINC00881knockdown significantly reduced peak calcium amplitude in the beating human iPSCs.ConclusionsFailing human heart exhibits etiology-specific changes in DNA methylation including coding and non-coding regions, which are minimally reversible with mechanical unloading. Epigenetic reprogramming may be necessary to achieve transcriptional normalization and sustained clinical recovery from heart failure.

IMPORTANCE Heart failure (HF) is often characterized by an insidious disease course leading to frequent rehospitalizations and a high use of ambulatory care. Remote cardiac monitoring is a promising approach to detect worsening HF early and intervene prior to an overt decompensation. OBSERVATIONS Recently, a multitude of novel technologies for remote cardiac monitoring (RCM) in patients with HF have been developed and are undergoing clinical trials. This development has been accelerated by the COVID-19 pandemic. CONCLUSIONS AND RELEVANCE This review summarizes the major clinical trials on RCM in patients with HF and present the most recent developments in noninvasive and invasive RCM technologies.

The publisher regrets that the original article was published without supplementary materials. The supplementary materials can now be found online at https://www.sciencedirect.com/science/article/pii/S0002914922003344?via%3Dihub.The publisher would like to apologise for any inconvenience caused. The publisher regrets that the original article was published without supplementary materials. The supplementary materials can now be found online at https://www.sciencedirect.com/science/article/pii/S0002914922003344?via%3Dihub. The publisher would like to apologise for any inconvenience caused. Meta-Analysis of Point-of-Care Lung Ultrasonography Versus Chest Radiography in Adults With Symptoms of Acute Decompensated Heart FailureAmerican Journal of CardiologyVol. 174PreviewAcute decompensated heart failure (ADHF) is a primary cause of older adults presenting to the emergency department with acute dyspnea. Point-of-care lung ultrasound (LUS) has shown comparable or superior diagnostic accuracy in comparison with a chest x-ray (CXR) in patients presenting with symptoms of ADHF. The systematic review and meta-analysis aimed to elucidate the sensitivity and specificity of LUS in comparison with CXR for diagnosing ADHF and summarize the rapidly growing body of evidence in this domain. Full-Text PDF

PurposeArterial hypertension is a common comorbidity among heart transplant (HT) recipients. Post-HT hypertension (HTN) can contribute to graft dysfunction and has been associated with the development of cardiac allograft vasculopathy. However, the risk factors for and optimal management of post-HT HTN is not completely understood.MethodsRetrospective review of electronic medical records for patients undergoing HT at a large academic center between 1/2010 and 12/2017 was performed. Patients undergoing repeat HT were excluded from the analysis. HTN was defined by clinician documentation in the medical record and treatment with anti-hypertensive agents.Results280 HT patients were identified with a median follow-up of 5.1 (IQR 2.6-8.1) years. 128 (45.7%) had pre-transplant HTN and 198 (70.7%) patients had post-transplant HTN. Among the 152 patients without pre-transplant HTN, 81 (53.3 %) were diagnosed with new-onset HTN during a median follow-up of 6.3 (IQR 3.5-9.0) years. Median age of those with new-onset HTN was 54 (IQR 44-64) years, 21.0% were female, and 18.5% had ischemic cardiomyopathy. In multivariable analyses, male sex was associated with new-onset post-HT HTN (HR 2.52, CI 1.19-5.48, p=0.02, Table 1a). Among the 198 patients with post-transplant HTN, 84.2% were treated with a beta blocker, 52.0% with a potassium-sparing diuretic, and 51.0% with an ACE inhibitor or angiotensin II receptor blocker during follow-up (Table 1b).ConclusionArterial HTN is a common complication of HT, affecting over 70% of our cohort. Males may be at higher risk for developing new-onset HTN post-HT. Further studies are required to determine the optimal medical therapy for this select cohort of patients with hypertension. Arterial hypertension is a common comorbidity among heart transplant (HT) recipients. Post-HT hypertension (HTN) can contribute to graft dysfunction and has been associated with the development of cardiac allograft vasculopathy. However, the risk factors for and optimal management of post-HT HTN is not completely understood. Retrospective review of electronic medical records for patients undergoing HT at a large academic center between 1/2010 and 12/2017 was performed. Patients undergoing repeat HT were excluded from the analysis. HTN was defined by clinician documentation in the medical record and treatment with anti-hypertensive agents. 280 HT patients were identified with a median follow-up of 5.1 (IQR 2.6-8.1) years. 128 (45.7%) had pre-transplant HTN and 198 (70.7%) patients had post-transplant HTN. Among the 152 patients without pre-transplant HTN, 81 (53.3 %) were diagnosed with new-onset HTN during a median follow-up of 6.3 (IQR 3.5-9.0) years. Median age of those with new-onset HTN was 54 (IQR 44-64) years, 21.0% were female, and 18.5% had ischemic cardiomyopathy. In multivariable analyses, male sex was associated with new-onset post-HT HTN (HR 2.52, CI 1.19-5.48, p=0.02, Table 1a). Among the 198 patients with post-transplant HTN, 84.2% were treated with a beta blocker, 52.0% with a potassium-sparing diuretic, and 51.0% with an ACE inhibitor or angiotensin II receptor blocker during follow-up (Table 1b). Arterial HTN is a common complication of HT, affecting over 70% of our cohort. Males may be at higher risk for developing new-onset HTN post-HT. Further studies are required to determine the optimal medical therapy for this select cohort of patients with hypertension.

Purpose Continuous pulmonary artery (PA) pressure monitoring has proven its value in reducing heart failure and all-cause hospitalizations. Invasive hemodynamic testing has shown that exercise in HFrEF leads to a steep increase in PA pressures and this steep rise is independently associated with reduced peak Vo2. PA pressure response during exercise is likely more closely related to outcomes than resting hemodynamics in HF. The significance and potentially prognostic value of measuring PA pressures during CPET testing in AHF patients is currently unknown. In this feasibility-study we describe PA pressure curves during CPET in a cohort of advanced HF patients. Methods 7 advanced HF patients (Etiology: 4 NICM, 3 ICM; age 61 ± 12y; EF 28 ± 15%; 86% on beta blocker) with CardioMEMS device underwent standard stationary bike - CPET. PA pressures were measured at rest, every 2 minutes during exercise and during recovery. Results Max VO2 was 13.3±5.2 ml/kg/min; average duration of exercise was 8:56 min. Mean resting PA pressure was 12.5±5.2 mmHg. Mean peak PA pressure was 26.7±10 mmHg. Mean PA pressures increased on average by 2.5-fold (± 1.14) (Figure 1). The slope of mPAP rise was 3.33±2.1. mPAP uniformly returned to baseline values within 3 minutes of recovery. Pt. 3 was admitted 1 week after CPET testing with subacute worsening HF symptoms and underwent OHT, all other patients continue to follow at the centralized HF program at our institution. Conclusion PAP assessment using CardioMEMS is feasible during CPET. mPAP rose sharply during exercise. In HF patients with invasive PA pressure monitor devices, exercise PAP assessment may be a valuable tool to assess for functional capacity with possibly prognostic significance.

Acute decompensated heart failure (ADHF) is a primary cause of older adults presenting to the emergency department with acute dyspnea. Point-of-care lung ultrasound (LUS) has shown comparable or superior diagnostic accuracy in comparison with a chest x-ray (CXR) in patients presenting with symptoms of ADHF. The systematic review and meta-analysis aimed to elucidate the sensitivity and specificity of LUS in comparison with CXR for diagnosing ADHF and summarize the rapidly growing body of evidence in this domain. A total of 5 databases were searched through February 18, 2021, to identify observational studies that reported on the use of LUS compared with CXR in diagnosing ADHF in patients presenting with shortness of breath. Meta-analysis was conducted on the sensitivities and specificities of each diagnostic method. A total of 8 studies reporting on 2,787 patients were included in this meta-analysis. For patients presenting with signs and symptoms of ADHF, LUS was found to be more sensitive than CXR (91.8% vs 76.5%) and more specific than CXR (92.3% vs 87.0%) for the detection of cardiogenic pulmonary edema. In conclusion, LUS is more sensitive and specific than CXR in detecting pulmonary edema. This highlights the importance of sonographic B-lines, along with the accurate interpretation of clinical data, in the diagnosis of ADHF. In addition to its convenience, reduced costs, and reduced radiation exposure, LUS should be considered an effective alternative to CXR for evaluating patients with dyspnea in the setting of ADHF. (C) 2022 Elsevier Inc. All rights reserved.

Background Human heart failure is characterized by global alterations in the myocardial DNA methylation profile, yet little is known about epigenetic regulation of non-coding transcripts and potential reversibility of DNA methylation with left ventricular assist device (LVAD) support. Method Genome-wide mapping of myocardial DNA methylation was performed in 36 patients with end-stage heart failure at the time of LVAD implant, 8 patients at the time of LVAD explant, and 7 non-failing controls using high-density bead array platform. Transcriptomic and functional studies were performed in human induced pluripotent stem cell derived cardiomyocytes (iPSCs). Results Etiology-specific analysis revealed 2079 differentially methylated positions (DMPs) in ischemic cardiomyopathy (ICM) and 261 DMPs in non-ischemic cardiomyopathy (NICM). 192 DMPs were common to ICM and NICM. Analysis of paired samples before and after LVAD support demonstrated reverse methylation of only 3.2% of HF-specific DMPs. Methylation-expression correlation analysis yielded several protein-coding genes that are hypomethylated and upregulated ( HTRA1, FAM65A, FBXO16, EFCAB13, AKAP13, RPTOR ) or hypermethylated and downregulated ( TBX3 ) in ICM and NICM patients. A novel cardiac-specific super-enhancer lncRNA ( LINC00881 ) is hypermethylated and downregulated in the failing human heart. LINC00881 is an upstream regulator of sarcomere and calcium channel gene expression including MYH6, CACNA1C , and RYR2. LINC00881 knockdown significantly reduced peak calcium amplitude in the beating human iPSCs. Conclusions Failing human heart exhibits etiology-specific changes in DNA methylation including coding and non-coding regions, which are minimally reversible with mechanical unloading. Epigenetic reprogramming may be necessary to achieve transcriptional normalization and sustained clinical recovery from heart failure. ### Competing Interest Statement The authors have declared no competing interest.

Purpose New-onset post-transplantation diabetes mellitus (DM) is common among heart transplant (HT) recipients and has been shown to be associated with higher rates of renal dysfunction and death or re-transplantation. There are limited data to describe the use of novel anti-diabetic therapies in this population. We aimed to describe the prevalence of newly diagnosed DM and DM treatment patterns in HT patients at a single high-volume transplant center. Methods Patients undergoing HT between 1/2010-12/2017 were retrospectively reviewed. Patients undergoing repeat HT were excluded from the analysis. New-onset DM was defined by HbA1c >= 6.5% or initiation of anti-diabetic therapy. Data were collected from the electronic medical record. Results 280 transplant patients were identified with a median follow-up of 5.1 (IQR 2.6-8.1) years. 95 (33.9%) had pre-transplant DM. Of the 185 remaining patients, 45 (24.3%) developed post-HT DM with a median time to diagnosis of 109 (IQR 20-439) days. Median age of those with new-onset DM was 54 (IQR 47-61) years and 37.8% were female. Risk of PTDM was 18.2% at 1 year, 20.0% at 2 years, 23.8% at 5 years, and 33.1% at 10 years (Fig 1a). Hypertension was independently associated with post-HT DM (p = 0.014, Fig 1b). Among all patients with DM in the post-transplant period (N=140), 10 (7.1%) were started on a sodium-glucose cotransporter-2 inhibitor (SGLT2i) and 17 (12.1%) were treated with a glucagon-like peptide-1 receptor agonist (GLP-1 RA). Adverse events with SGLT2i included polyuria in 2 patients, and adverse events with GLP-1 RA included gastrointestinal disturbance in 2 patients, palpitations in 1 patient, and discontinuation for unknown reasons in 1 patient. Conclusion DM is a common co-morbidity among HT recipients, with a high rate of pre-existing DM and post-HT DM. Utilization of the newest anti-diabetic agents with known cardiovascular benefits remains low in this cohort.

Purpose The Impella 5.5 system is the newest temporary left ventricular assist device (LVAD) for the treatment of cardiogenic shock (CS). Impella 5.5 aims to improve deliverability and durability over Impella 5.0, but real-world experience with this device is limited. We aimed to report our clinical experience with Impella 5.5. Methods Clinical and outcome data of all patients treated with Impella 5.5 at our center between Feb and Oct 2020 were collected. AKI was defined as per KDIGO criteria, vascular complications as per VARC-2 criteria and severe thrombocytopenia as <50k. Results 13 patients with Impella 5.5 were managed at our center (9 (69%) male, median age 58y (IQR 52, 67). 5 patients were transitioned to Impella 5.5 from VA-ECMO, 2 from Impella CP, 2 from IABP, and 4 from inotropes. Etiology of CS was AMI in 6 cases, decompensated chronic HF in 5, suspected acute myocarditis in 1 and post-cardiotomy CS in 1 case. Median duration of Impella 5.5 support was 12 days (IQR 7-28). 2 patients required device removal due to complications: 1 with entanglement in the mitral subvalvular apparatus, 1 with migration into the ascending aorta. Device-related complications were hemolysis in 4 (30%) patients, severe thrombocytopenia in 1, axillary hematoma (minor as per VARC-2 criteria) in 3 (23%), and AKI in 2 patients (15%). No stroke, valve injury or limb complications occurred. Survival to device explant was 85%. 2 patients who were not candidates for durable LVAD or transplant died on support of refractory CS. Of the survivors, 2 required surgically implanted biventricular support for refractory ventricular arrhythmia, 4 were bridged to durable VAD, 2 were bridged to OHT, and 3 achieved ventricular recovery. At the time of analysis, 3 patients remain hospitalized (1 surgical BIVAD, 1 early post-durable LVAD, 1 recovered after device explant). Conclusion All patients supported with Impella 5.5 were critically ill in profound CS. Rates of procedural and device-related complications were favorable, and survival was high in this critically ill cohort.

AIMS:Allograft rejection following heart transplantation (HTx) is a serious complication even in the era of modern immunosuppressive regimens and causes up to a third of early deaths after HTx. Allograft rejection is mediated by a cascade of immune mechanisms leading to acute cellular rejection (ACR) and/or antibody-mediated rejection (AMR). The gold standard for monitoring allograft rejection is invasive endomyocardial biopsy that exposes patients to complications. Little is known about the potential of circulating miRNAs as biomarkers to detect cardiac allograft rejection. We here present a systematic analysis of circulating miRNAs as biomarkers and predictors for allograft rejection after HTx using next-generation small RNA sequencing.METHODS AND RESULTS:We used next-generation small RNA sequencing to investigate circulating miRNAs among HTx recipients (10 healthy controls, 10 heart failure patients, 13 ACR, and 10 AMR). MiRNA profiling was performed at different time points before, during, and after resolution of the rejection episode. We found three miRNAs with significantly increased serum levels in patients with biopsy-proven cardiac rejection when compared with patients without rejection: hsa-miR-139-5p, hsa-miR-151a-5p, and hsa-miR-186-5p. We identified miRNAs that may serve as potential predictors for the subsequent development of ACR: hsa-miR-29c-3p (ACR) and hsa-miR-486-5p (AMR). Overall, hsa-miR-486-5p was most strongly associated with acute rejection episodes.CONCLUSIONS:Monitoring cardiac allograft rejection using circulating miRNAs might represent an alternative strategy to invasive endomyocardial biopsy.

MiRNA-regulated processes are pivotal in cardiovascular homeostasis and disease. These short non-coding RNAs have ideal properties that could be utilized as potential biomarkers; moreover, their functions as post-transcriptional regulators of mRNA make them interesting therapeutic targets. In this review, we summarize the current state of miRNA-based biomarkers in a variety of diseases leading to heart failure, as well as provide an outlook on developing miRNA-based therapies in the heart failure field.

Abstract Aims We aimed to detail the early clinical experience with pVAD 5.5 at a large academic medical centre. Impella® 5.5 (Abiomed) is a temporary peripherally inserted left ventricular assist device (pVAD) used for the treatment of cardiogenic shock (CS). This system has several modifications aimed at improving deliverability and durability over the pVAD 5.0 system, but real‐world experience with this device remains limited. Methods and results We collected clinical and outcome data on all patients supported with pVAD 5.5 at our centre between February and December 2020, including procedural and device‐related complications. Fourteen patients with pVAD 5.5 were included. Aetiology of CS was acute myocardial infarction (n = 6), decompensated heart failure (n = 6), suspected myocarditis (n = 1), and post‐cardiotomy CS (n = 1). Four patients received pVAD 5.5 after being on inotropes alone, two were escalated from intra‐aortic balloon pump, two were escalated from pVAD CP, and six patients were transitioned to pVAD 5.5 from extracorporeal membrane oxygenation. Median duration of pVAD 5.5 support was 12 (interquartile range 7, 25) days. Complications included axillary insertion site haematoma (n = 3), acute kidney injury (n = 3), severe thrombocytopenia (n = 1), and stroke (n = 1). No valve injury or limb complications occurred. Survival to device explant for recovery or transition to another therapy was 11/14 (79%) patients. Conclusions In this early experience of the pVAD 5.5, procedural and device‐related complications were observed but were manageable, and overall survival was high in this critically ill cohort, particularly when the device was used as a bridge to other therapies.

Background Presentation of life-threatening arrhythmias concomitantly with a new-onset non-ischaemic cardiomyopathy raises concern for an inflammatory cardiomyopathy such as cardiac sarcoidosis or cardiac manifestations of connective tissue disease. Comprehensive workup for specific aetiologies may be unrevealing except for signs of myocardial inflammation identified on cardiac positron emission tomography (PET). Here, we present five cases of such subjects and their clinical course. Case summary We collected clinical, imaging, pathological, and follow-up data of five subjects presenting with arrhythmias and unexplained new-onset cardiomyopathy. Mean age was 56.2 +/- 5.8 years. Three subjects presented with ventricular tachycardia and two with atrial arrhythmias. Echocardiography showed a mean left ventricular ejection fraction of 37 +/- 9%. Significant coronary artery disease was ruled out in all cases as the cause of the cardiomyopathy. All patients underwent cardiac magnetic resonance imaging (MRI) and PET scan at presentation and follow-up. In all patients, cardiac MRI revealed hyperenhancement in epicardial and mid-myocardial pattern in a non-coronary distribution, while PET scan revealed fluorodeoxyglucose (FDG) mismatch defects in multiple foci in a non-coronary distribution. Right ventricular biopsy was obtained in all patients and revealed interstitial fibrosis and cardiomyocyte hypertrophy. On median follow-up of 210 days, all subjects had improvement in both heart failure symptoms and arrhythmias and repeat PET in four out of five patients showed decreased inflammation. Discussion A high level of suspicion for inflammatory cardiomyopathy is needed in patients presenting with new unexplained cardiomyopathy and arrhythmias. A cardiac FDG-PET should be considered for diagnosis if cardiac inflammation is in the differential. This can inform further decisions regarding targeted immunomodulation therapy that may be helpful in this cohort.

Objective To quantify differences in the diagnosis and treatment of heart failure with preserved ejection fraction (HFpEF) between cardiologists and noncardiologists, who often diagnose and manage HFpEF. Methods Cardiologists and noncardiologists (internal medicine, medicine/pediatrics, family medicine, geriatrics) were anonymously surveyed between January 16, 2018, and March 2, 2018, regarding practices related to diagnosing and managing HFpEF at the University of Michigan and Weill Cornell Medical Center. Response data were compared using χ2 analysis. Results Of 1010 physicians surveyed, 211 completed a significant portion of the survey: 32 cardiologists and 179 noncardiologists. Most noncardiologists were unaware of HFpEF diagnostic guidelines and commonly used left ventricular diastolic dysfunction and natriuretic peptides to diagnose HFpEF. Noncardiologists (32.3%, n=52) were less likely than cardiologists (64.5%, n=20) to prescribe an aldosterone antagonist for HFpEF (P=.001). Both groups reported similar use of β-blockers, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, and exercise programs. Noncardiologists were more likely to refer patients with HFrEF to cardiology (63.1%, n=111) compared with patients with HFpEF (33.5%, n=59; P<.001). Noncardiologists were more likely to discuss prognosis and goals of care with patients with HFrEF (84.4%, n=151) than with patients with HFpEF (65.9%, n=118; P<.001). Conclusion Cardiologists and noncardiologists vary significantly in their HFpEF diagnosis and treatment practices. As diagnostic criteria continue to be evaluated for HFpEF, dissemination of these guidelines to noncardiologists, with an emphasis on the morbidity and mortality associated with HFpEF, is imperative.