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Patients with significant mitralregurgitation (MR) often experience atrial fibrillation (AF). The effects of transcatheter edge-to-edge repair (TEER) for MR on AF burden is unknown.Patients who underwent TEER atthree institutions who also had a cardiac implantable electronic device with aright atrial lead were retrospectively identified. In patients with baseline AF, device data onAF burden and echocardiographic changes were recorded at baseline and 3- and 12-month follow up time points when available. Data is expressed as number (%) and median (interquartile range), withpaired values analyzed using the Wilcoxon signed-rank test.Overall 66 patients wereidentified, of whom 54 (82%) had baseline data on AF available for review. Of these, 18 (33%) had a baseline burden ofAF (median burden 100% [54-100%]). Patients were 77 (71-83) years old, 10 (56%) male, 14 (78%) White, and 3 (17%) Black. A significant reduction in AF burdenwas observed at 3 months (11 patients, p = 0.03) which did not retainsignificance at 12 months (8 patients, p = 0.69). Indexed maximal left atrial volumes did not significantly change inthose with paired studies available (p0.35 for both time points).In this multicenter cohort, one thirdof patients with severe MR undergoing TEER had an AF burden at baseline, whichwas found to be significantly lower at 3 month follow up. Further investigation is needed to confirm thefindings of this small cohort and determine its effects on downstream sequelaeof AF.

Vasodilator stress cardiovascular magnetic resonance (CMR) is a powerful diagnostic modality, but data toward its use in patients with permanent pacemakers (PPMs) or implantable cardioverter-defibrillators (ICDs) is limited.Patients with ICDs (1% pacing) or PPMs who underwent regadenoson single photon emission computed tomography (SPECT) and all patients with ICDs or PPMs who underwent stress CMR were retrospectively identified. SPECT tests were analyzed for hemodynamic responses and new pacing requirements; CMR studies were examined for safety, device characteristics and programming, hemodynamic responses, and image quality. Changes from baseline were evaluated with the Related-Samples Wilcoxon Signed Rank Test. Of 67 patients (median age 65 [IQR 58-72] years, 31 [46%] female, 31 [46%] Black), 47 underwent SPECT and 20 CMR. With regadenoson SPECT, 89% of patients experienced tachycardic responses above resting heart rates (+19 [13-32] beats per minute, p .01). During stress CMR, 10 (50%) devices were asynchronously paced approximately 10 beats per minute above resting rates, and the remaining were temporarily deactivated. Those with asynchronous pacing had no changes in heart rates, whereas patients with deactivated devices had near uniform heart rate accelerations. Image quality was diagnostic in the majority of stress CMR sequences, with nonconditional ICDs contributing 40 of 57 (70%) of nondiagnostic segments.This data supports the safety of vasodilator stress CMR with promising diagnostic quality images in patients with CMR conditional ICDs and PPMs. Despite a near uniform tachycardic response to regadenoson in the SPECT environment, high rates of asynchronous pacing during vasodilator stress CMR did not result in competitive pacing or adverse arrhythmic events. Further studies are needed to validate these findings and confirm the diagnostic and prognostic performance of stress CMR in these individuals.

There is limited understanding on the potential differences in the pathophysiology between de novo heart failure with reduced ejection fraction (HFrEF) and acute on chronic HFrEF. The aim of this study was to assess differences in cardiorespiratory fitness (CRF) parameters between de novo heart failure and acute on chronic HFrEF using cardiopulmonary exercise testing (CPX). We retrospectively analyzed CPX data measured within 2 weeks of discharge following acute hospitalization for HFrEF. Data are reported as median and interquartile range or frequency and percentage (%). We included 102 patients: 32 (31%) women, 81 (79%) black, 57 [51–64] years of age, BMI of 34 [29–39] Kg/m(2). Of these, 26 (25%) had de novo HFrEF and 76 (75%) had acute on chronic HFrEF. When compared with acute on chronic, patients with de novo HFrEF had a significantly higher peak oxygen consumption (VO(2)) (16.5 [12.2–19.4] vs 12.8 [10.1 15.3] mL·kg(−1) min (−1), p

Aims ST-segment elevation myocardial infarction (STEMI) is associated with an intense acute inflammatory response and an increased risk of death and heart failure (HF). In this study, we sought to evaluate the effect of anakinra, a recombinant interleukin-1 receptor antagonist, on the incidence of HF. Methods and results We performed a pooled analysis of three early phase randomized clinical trials. The endpoints included the composite of all-cause death and new-onset HF, and the composite of all-cause death and hospitalization for HF at 1-year follow-up. Safety events, including injection site reaction and serious infections, were also recorded. We analysed 139 patients with STEMI from three separate trials: VCUART (N = 10), VCUART2 (N = 30), and VCUART3 (N = 99). Of these, 84 (60%) patients were randomized to anakinra and 55 (40%) to placebo. Treatment with anakinra significantly reduced the incidence of all-cause death or new-onset HF (7 [8.2%] vs. 16 [29.1%], log-rank P = 0.002) and of all-cause death or HF hospitalization (0 [0] vs. 5 [9.1%], log-rank P = 0.007). Patients treated with anakinra had significantly higher injection site reactions (19 [22.6%] vs. 3 [5.5%], P = 0.016) without a significant difference in the incidence of serious infections (11 [13.1%] vs. 7 [12.7%], P = 0.435). Treatment with anakinra significantly reduced the area under the curve for high-sensitivity C-reactive protein between baseline and 14 days (75.48 [41.7–147.47] vs. 222.82 [117.22–399.28] mg day/L, P Conclusion IL-1 blockade with anakinra for 14 days in patients with STEMI reduces the incidence of new-onset HF or hospitalization for HF at 1 year following STEMI.

The sodium glucose co-transporter 2 inhibitors have demonstrated favorable effects on cardiovascular and renal disease; however, they may also increase low-density lipoprotein cholesterol (LDL-C). There are limited data directly comparing the effects of sodium glucose co-transporter 2inhibitors on serum lipids to other antihyperglycemic therapies. In this post-hoc analysis of the CANA-HF trial, we sought to compare the effects of canagliflozin to sitagliptin in patients with type 2 diabetes mellitus (T2DM) and heart failure and reduced ejection fraction (HFrEF). The CANA-HF trial was a prospective, randomized controlled study that compared the effects of canagliflozin 100 mg daily to sitagliptin 100 mg daily on cardiorespiratory fitness in patients with HFrEF and T2DM. Of the 36 patients enrolled in CANA-HF, 35 patients had both baseline and 12-weeks serum lipids obtained via venipuncture. The change in LDL-C from baseline to 12 weeks was 5 (-12.5 to 19.5) mg/dL versus -8 (-19 to -1) mg/dL (P = 0.82) and triglyceride levels was -4 (-26 to 9) mg/dL and -10.5 (-50 to 29.3) mg/dL (P = 0.52) for canagliflozin and sitagliptin, respectively. No significant differences were found between canagliflozin and sitagliptin for total cholesterol, high-density lipoprotein cholesterol or non-HDL-C (P > 0.5 for all). These data suggest that compared with sitagliptin, canagliflozin may not increase LDL-C in patients with T2DM and HFrEF.

Background: Sarcopenia impairs cardiorespiratory fitness (CRF) in patients with heart failure with reduced ejection fraction (HFrEF). Obesity has also been shown to impair CRF; however, the effects of sarcopenia on CRF in patients with obesity and HFrEF are unknown. The aim of this analysis was to examine differences in CRF between patients with sarcopenic obesity (SO) and non-SO (NSO) with HFrEF. We also assessed associations between skeletal muscle mass index (SMMI) and CRF. Methods: Forty patients with HFrEF and obesity underwent cardiopulmonary exercise testing to collect measures of CRF including peak oxygen consumption (VO 2 ), circulatory power, oxygen uptake efficiency slope, O 2 pulse, and exercise time. Body composition was performed in all patients using bioelectrical impedance analysis to quantify fat mass index and divide patients into SO and NSO based on SMMI cutoffs. Results are presented as mean (SD) or median [interquartile range] as appropriate. Results: Nearly half (43% [n=17]) of patients had SO. Patients with SO had a lower SMMI than those with NSO, and no differences in fat mass index were observed between groups. Those with SO achieved a lower absolute peak VO 2 (NSO, 1.62±0.53 L·min -1 versus SO, 1.27±0.44 L·min -1 , P =0.035), oxygen uptake efficiency slope (NSO, 1.92±0.59 versus SO, 1.54±0.48, P =0.036), and exercise time (NSO, 549±198 seconds versus SO, 413±140 seconds, P =0.021) compared to those with NSO. On multivariate analysis, SMMI remained a significant predictor of absolute peak VO 2 when adjusted for age, sex, adiposity, and HF severity. Conclusions: In patients with HFrEF and obesity, sarcopenia, defined as low SMMI, is associated with a clinically significant reduction in CRF, independent of adiposity.

Myocarditis is associated with numerous infectious and noninfectious triggers; cardiovascular magnetic resonance imaging during and after the episode may inform prognosis ([1][1]). Criteria for myocarditis include abnormal T1 and T2 findings, the latter identifying active inflammation or edema ([2][

"Cardiac imaging is an essential tool in the field of cardio-oncology. Cardiovascular magnetic resonance (CMR) stands out for its accuracy, reproducibility, and ability to provide tissue characterization. These attributes are particularly helpful in screening and diagnosing cardiotoxicity, infiltrative disease, and inflammatory cardiac disease. The ability of CMR to detect subtle changes in cardiac function and tissue composition has made it a useful tool for understanding the pathophysiology of cardiotoxicity. Because of these unique features, CMR is gaining prominence in both the clinical and research aspects of cardio-oncology."

Background Patients with malignancy who experience metastasis to cardiac structures may exhibit ST-segment elevations and acute coronary syndrome (ACS) through poorly understood pathophysiologic mechanisms. We present a case in which vasodilator stress cardiovascular magnetic resonance provides unique insight into one such patient who suffered from recurrent episodes resembling ACS. Case summary A 58-year-old male with metastatic lung adenocarcinoma presented with refractory angina and dynamic inferior electrocardiogram changes. The patient was referred for adenosine stress cardiovascular magnetic resonance, revealing multiple territories of abnormal perfusion during rest with improvement during adenosine infusion. Subsequent computed tomography displayed tumour encasement of the right coronary artery. Taken together, vasodilator-responsive extrinsic compression of multiple epicardial coronary arteries was suspected. Outpatient oncology follow-up for chemoimmunotherapy initiation was arranged with the hope that reducing tumour burden might alleviate coronary compression. However, in the ensuing months, the patient’s disease advanced beyond the point of which his symptoms could be controlled medically, and he was ultimately enrolled in hospice care. Discussion Encasement of coronary arteries can result in anginal symptoms if their position impairs coronary arterial flow. The presented case highlights the unique manner in which these lesions might behave on stress cardiac magnetic resonance imaging. Clinicians who encounter such unusual findings on vasodilator stress imaging should consider metastatic lesions to the cardiac structures on the differential diagnosis.

Cardiorespiratory fitness (CRF) is now established as a vital sign. Cardiopulmonary exercise testing (CPX) is the gold-standard approach to assessing CRF.A body of literature spanning several decades clearly supports the clinical utility of CPX in those who are apparently health and at risk for chronic disease as well as numerous patient populations. While CPX, in and of itself, is a valid and reliable clinical assessment, combining findings with other available assessments may provide a more comprehensive perspective that enhances clinical decision making and outcomes. The current review will accomplish the following: (1) define key CPX measures based upon current evidence; and (2) describe the current evidence addressing the relationships between CPX and echocardiography, serum biomarkers, and cardiovascular magnetic resonance.Cardiopulmonary exercise testing provides prognostic and diagnostic information in apparently healthy individuals, those at risk for one or more chronic conditions, as well as numerous patient populations. Moreover, if the goal of an intervention is to improve one or more systems integral to the physiologic response to exercise, CPX should be considered as a central assessment to gauge therapeutic efficacy. To further refine the information obtained from CPX, combining other assessments has demonstrated promise.

Impaired cardiorespiratory fitness (CRF) in heart failure (HF) is influenced by a complex array of cardiac and extracardiac factors. The study aimed to identify clinical determinants of CRF measured as peak oxygen consumption (peak VO2) in HF patients, and to determine a peak VO2 prediction model using regression equations. Retrospective analysis of 200 HF patients who completed treadmill cardiopulmonary exercise testing and underwent Doppler echocardiography and/or biomarker analysis on the same day was performed. After univariate linear regression analysis, a multivariate peak VO2 prediction model was developed using significant variables in a stepwise linear regression analysis. In subjects with repeated testing, Pearson's correlation was used to assess correlations between measured and predicted change in peak VO2 (Δpeak VO2) over time. Mean age was 57 years, with 55% being male. Stepwise linear regression was used to generate a weighted model for peak VO2: 30.895 + (−0.112•age[years]) + (0.296•hemoglobin [g/dl]) + (−0.101•E/e'[unit change]) + (−0.202• body mass index [kg/m2]) + (−0.593• N-terminal pro-brain natriuretic peptide [logN pg/ml])) + (−1.349•CRP [log mg/L]). Predicted peak VO2 correlated strongly with measured peak VO2 in HF with reduced ejection fraction and HF with preserved ejection fraction patients (r = +0.63, p 2 correlated with measured Δpeak VO2 (r = +0.23, p 2 in HF patients and may be used to estimate peak VO2 changes over time.

BACKGROUND The risk of adverse cardiovascular events in patients with acute myocarditis (AM) and desmosomal gene variants (DGV) remains unknown.OBJECTIVES The purpose of this study was to ascertain the risk of death, ventricular arrhythmias, recurrent myocarditis, and heart failure (main endpoint) in patients with AM and pathogenic or likely pathogenetic DGV.METHODS In a retrospective international study from 23 hospitals, 97 patients were included: 36 with AM and DGV (DGV[+]), 25 with AM and negative gene testing (DGV[-]), and 36 with AM without genetics testing. All patients had troponin elevation plus findings consistent with AM on histology or at cardiac magnetic resonance (CMR). In 86 patients, CMR changes in function and structure were re-assessed at follow-up.RESULTS In the DGV(+) AM group (88.9% DSP variants), median age was 24 years, 91.7% presented with chest pain, and median left ventricular ejection fraction (LVEF) was 56% on CMR (P = NS vs the other 2 groups). Kaplan-Meier curves demonstrated a higher risk of the main endpoint in DGV(+) AM compared with DGV(-) and without genetics testing patients (62.3% vs 17.5% vs 5.3% at 5 years, respectively; P < 0.0001), driven by myocarditis recurrence and ventricular arrhythmias. At follow-up CMR, a higher number of late gadolinium enhanced segments was found in DGV(+) AM. CONCLUSIONS Patients with AM and evidence of DGV have a higher incidence of adverse cardiovascular events compared with patients with AM without DGV. Further prospective studies are needed to ascertain if genetic testing might improve risk stratification of patients with AM who are considered at low risk. (J Am Coll Cardiol HF 2022;10:714-727) (c) 2022 by the American College of Cardiology Foundation.

Hypothesis: There is limited understanding on the potential differences in the pathophysiology between de-novo heart failure with reduced ejection fraction (HFrEF) and acute on chronic HFrEF. Objective: the aim of this study was to assess differences in cardiorespiratory fitness (CRF) parameters between de-novo heart failure and acute on chronic HFrEF using cardiopulmonary exercise testing (CPX). Methods: We retrospectively analyzed CPX data measured within 2 weeks of discharge following acute hospitalization for HFrEF. The predicted peak oxygen consumption (VO 2 ) was calculated using the FRIEND formula. Circulatory power, a measure of cardiac reserve, was calculated as the product of peak VO 2 and peak systolic blood pressure. Peak O 2 pulse, a surrogate measure of exercise stroke volume, was calculated by dividing peak VO 2 by the maximum heart rate (HR). Left ventricular ejection fraction (LVEF) was calculated using Simpson method during echocardiography. Data are reported as median and interquartile range or frequency and percentage (%). Results: We included 102 patients: 32 (31%) women, 81 (79%) Black, 57.0 [ 51-64] years of age, BMI of 34 [29-39] Kg/m 2 . Of these, 26 (25%) had de-novo HFrEF and 76 (75%) had acute on chronic HFrEF. When compared with acute on chronic, patients with de-novo HFrEF had a significantly higher peak VO 2 (16.5 [12.2-19.4] vs 12.8 [10.15-15.32] mL·kg -1 ·min -1 , p 2 (58% [51-75] vs 49% [42-59]) p =0.012), peak HR (134 [117-147] vs 117 [104-136] bpm, p =0.004), peak O 2 pulse (12.2 [10.5 -15.5] vs 9.9 [8.0-13.1] mL/beat, p =0.022) and circulatory power (2823 [1973-3299] vs 1902 [1372-2512] mmHg·mL·kg -1 ·min -1 , p=0.002). No significant difference in resting LVEF was found between groups. Conclusion: Patients with de-novo HFrEF patients have better CRF parameters than those with acute on chronic HFrEF. These differences are not explained by resting left ventricular systolic function but may be related to greater preservation in cardiac reserve during exercise in de-novo HFrEF patients.

Background. Leukocytosis is a common finding in patients with ST elevation myocardial infarction (STEMI) and portends a poor prognosis. Interleukin 1-b regulates leukopoiesis and pre-clinical studies suggest that anakinra (recombinant human interleukin-1 [IL-1] receptor antagonist) suppresses leukocytosis in myocardial infarction. However, the effect of IL-1 blockade with anakinra on leukocyte count in patients with STEMI is unknown. Methods. We reviewed the white blood cell (WBC) and differential count of 99 patients enrolled in a clinical trial of anakinra (n=64) versus placebo (n=35) for 14 days after STEMI. A complete blood cell count with differential count were obtained at admission, and after 72 hours, 14 days and 3 months.Results. After 72 hours from treatment, anakinra compared to placebo led to a statistically significant greater percent reduction in total WBC count (-35% [-48 to -24] vs -21% [-34 to -10], P=0.008), absolute neutrophil count (-48% [-60 to -22] vs -27% [-46 to -5], P=0.004) and to an increase in absolute eosinophil count (+50% [0 to +100] vs 0% [-50 to +62], P=0.022). These changes persisted while on treatment at 14 days and were no longer apparent at 3 months after treatment discontinuation. Conclusion. We found that in patients with STEMI IL-1 blockade with anakinra accelerates resolution of leukocytosis and neutrophilia. This modulation may represent one of the mechanisms by which IL-1 blockade improves clinical outcomes.

Cardiorespiratory fitness (CRF) is a robust and independent predictor of cardiovascular health and overall mortality. Patients with lung cancer often have chronic lung disease, contributing to impaired CRF. Radiation to the heart during lung cancer treatment may further reduce CRF. The determinants of CRF in this population are not well understood. We prospectively evaluated 12 patients with lung cancer without known cardiovascular disease with reduced lung function receiving curative intent thoracic radiotherapy to determine whether cardiac diastolic function, as assessed by Doppler echocardiography and N-terminal pro-brain natriuretic peptide (NTproBNP) levels, correlate with CRF measured by peak oxygen consumption (VO(2)). Doppler-derived measures of diastolic function and serum NTproBNP levels inversely correlated with peak VO(2.) In a multivariate regression model, NTproBNP was the strongest independent variable associated with peak VO(2). These results suggest that diastolic dysfunction further contributes to reduced CRF in patients with lung cancer who have received radiotherapy.

Decompensated cirrhosis is associated with high morbidity and mortality in the absence of liver transplantation (LT) [(1)][1]. LT is a high-risk surgery, and all potential LT waitlist registrants undergo extensive workup to assess and optimize their surgical risk; an integral part of this is cardiac

Alirocumab improves outcomes in patients with a history of recent acute coronary syndrome, but treatment acutely at the time of myocardial infarction is untested. We present the results of a randomized, placebo-controlled, double-blinded pilot study of alirocumab treatment at the time of non-ST elevation MI (NSTEMI). Twenty patients with type 1 NSTEMI and low-density lipoprotein cholesterol (LDL-C) >70 mg/dL despite high intensity statin therapy were randomized 1:1 to one dose of alirocumab 150 mg subcutaneously or placebo within 24 hours of presentation. LDL-C and inflammatory biomarkers—including C-reactive protein—were obtained at baseline, 72 hours, and 14 days. Median (interquartile range) and number (%) were: age 59 (49, 65) years, 7 (35%) men, 16 (80%) black; baseline characteristics were similar between groups. Alirocumab significantly reduced LDL-C from baseline to 14 days by 64 mg/dL (−96, −47) compared with placebo [+1 mg/dL (−25, +16)] (primary endpoint). There were no significant between-group differences in C-reactive protein changes at any time point (all P > 0.2) or serious adverse events attributable to the study treatment. In conclusion, alirocumab administration at the time of NSTEMI significantly reduced LDL-C levels at 14 days, was safe, and had neutral effects on inflammatory biomarkers. Further studies are warranted to explore the effects on clinical outcomes.

The purpose of this study was to determine the relationship between liver histology, exercise tolerance and diastolic function in patients with nonalcoholic fatty liver disease (NAFLD). Myocardial remodeling and diastolic dysfunction have been associated with NAFLD. However, its physiological impact and relationship to the histological severity of NAFLD is not known. Cardiopulmonary exercise testing and stress echocardiography was performed in subjects with biopsy-confirmed NAFLD. Maximal aerobic exercise capacity (peak oxygen consumption [VO(2)]) was related to diastolic function (mitral annulus Doppler velocity e’ and ratio of early diastolic filling pressure [E] to e’ [E/e’]) at rest and peak exercise. Autonomic dysfunction was determined from heart rate recovery after exercise. Independent predictors of cardiac function and exercise capacity were identified by multivariable regression. Thirty-six subjects (nonalcoholic fatty liver [NAFL=15], nonalcoholic steatohepatitis [NASH=21]) were enrolled. NASH was associated with impaired exercise capacity compared to NAFL (median peak VO(2) 17.0 [15.4, 18.9] vs. 19.9 [17.4, 26.0], P=001); pVO(2) declined with increasing fibrosis (F0=22.5, F1=19.9, F2=19.0, F3=16.6 mlkg(−1)min(−1); P=0.01). Similarly, E/e’ during exercise increased progressively with increasing fibrosis (F0=5.6, F1=6.5, F2=8.7, F3=9.8; P=0.02). Finally, heart rate recovery, a marker of autonomic function, was blunted in those with higher fibrosis stages (F0=25 [20, 30], F1=23 [17.5, 27.0], F2=17 [11.8, 21.5], F3=11 [8.5, 18.0] beats per minute; P

Intracardiac thrombi can occur in a variety of locations and are frequently encountered in clinical practice. Yet evidence-based guidance for clinicians managing patients with intracardiac thrombi is often limited. This review summarizes what is known regarding the prevalence of intracardiac thrombus, diagnostic strategies, clinical relevance, and treatment options, focusing on four specific types of thrombus for which recent research has shifted clinical understanding and treatment decisions: (1) left atrial appendage thrombus, (2) cardiac implantable electronic device lead thrombus, (3) bioprosthetic aortic valve thrombus, and (4) left ventricular thrombus. Additional studies, ideally prospective, randomized, and head-to-head in design, are needed to better inform best practices in patients with intracardiac thrombi.

While pharmacologic stress cardiovascular magnetic resonance imaging (MRI) is a robust noninvasive tool in the diagnosis and prognostication of epicardial coronary artery disease, clinical guidelines recommend exercise-based testing in those patients who can exercise. This review describes the development of exercise cardiovascular MRI protocols, summarizes the insights across various patient populations, and highlights future research initiatives. LEVEL OF EVIDENCE: 5 TECHNICAL EFFICACY: Stage 2.

Background LVADs provide life-sustaining treatment for patients with heart failure, but their complexity allows for complications. One complication, LVAD outflow graft obstruction, may be misdiagnosed as intraluminal thrombus, when more often it is extraluminal compression from biodebris accumulation. It can often be treated endovascularly with stenting. This case series describes diagnostic and procedural techniques for the treatment of left ventricular assist device (LVAD) outflow graft obstruction. Methods We present four patients with LVADs who developed LVAD outflow graft obstruction within the bend relief-covered segment. All were initially diagnosed with computed tomographic angiography (CTA). All underwent invasive evaluation with intravascular ultrasound (IVUS), then were treated with stenting. After misdiagnosing a twist, we developed the technique of balloon "graftoplasty" to ensure suitability for stent delivery in subsequent cases. Results All patients presented with low-flow alarms and symptoms of low output, and were diagnosed with outflow graft obstruction by CTA. In all four, IVUS confirmed an extraluminal etiology. Patient 1 was treated with stenting and had a good outcome. Patient 2's obstruction was from twisting, rather than biodebris accumulation, and had sub-optimal stent expansion and ultimately required surgery. Balloon "graftoplasty" was used in subsequent cases to ensure subsequent stent expansion. Patients 3 and 4 were successfully stented. All improved after treatment. Conclusions In patients with LVAD outflow graft obstruction, IVUS can distinguish intraluminal thrombus from extraluminal compression. Balloon "graftoplasty" can ensure that the outflow graft will respond to stenting. Many cases of LVAD outflow graft obstruction should be amenable to endovascular treatment.

Purpose: Cardiopulmonary exercise testing (CPX) is a well-established assessment with important insight into prognosis and therapeutic efficacy in patients with heart failure (HF). Prior studies have identified several clinical differences between Black or African American (B-AA) and Caucasian patients with HF. Differences in key CPX responses between these two groups require further investigation. Methods: Using a database consisting of subjects with symptomatic HF who had undergone CPX for inclusion in various prospective randomized clinical trials, we identified 198 (n = 94 [47%] B-AA; n = 105 [53%] Caucasian) patients with a qualifying baseline CPX. Significant univariate predictors of peak oxygen uptake (Vo2peak) were included in a multivariate linear regression model. Results: When compared with Caucasian patients, B-AA were younger (mean ± SD = 54.8 ± 10.0 vs 57.9 ± 9.6 yr, P =.03), had higher C-reactive protein (CRP) (median [IQR] = 4.9 [2.3, 8.8] vs 1.9 [0.6, 5.5] mg/L, P 2peak (14.6 ± 3.9 vs 17.6 ± 4.8 mL·kg−1·min−1, P 2) slope (P =.14). The difference in Vo2peak between B-AA and Caucasian was largely attenuated after adjusting for age, body mass index, CRP, N-terminal pro-brain natriuretic peptide, hemoglobin, LVEF, and peak HR (14.1: 95% CI, 13.2-14.9 vs 15.6: 95% CI, 14.4-16.8 mL·kg−1·min−1, P =.053). Conclusions: Directly measured Vo2peak was significantly lower in B-AA than in Caucasians with HF. This is largely explained by differences in clinical characteristics, whereas no significant differences were observed in the Ve/Vco2 slope.

Background ST segment elevation myocardial infarction (STEMI) is associated with an intense acute inflammatory response and an increased risk of death and heart failure (HF). We analyzed the effect of recombinant interleukin-1 receptor antagonist (anakinra) 100 mg subcutaneous injection given once or twice daily for 14 days on the occurrence of HF in a pooled analysis of 3 clinical trials. Methods Enrollment criteria and study procedures were the same across the three studies. High-sensitivity C-reactive protein (CRP) was measured at baseline, 72 hours, and 14 days to construct an area under the curve (AUC0–14). Clinical events up to 1 year were adjudicated by an independent committee blinded to treatment allocation. Data for anakinra once daily and anakinra twice daily were pooled into a single anakinra group. CRP data are presented as median and interquartile range to allow for deviation from Gaussian distribution and non-parametric tests were used to evaluate differences between groups. Kaplan-Meier survival analyses were conducted and the intervention groups were compared using a log-rank test. Results Between 2008 and 2017, 139 patients with STEMI were enrolled. 84 patients were randomized to anakinra and 55 patients were randomized to placebo. Anakinra significantly reduced the CRP AUC0–14 (76 [42–147] vs 222 [117–339] mg*day/L; P Conclusions Treatment with anakinra for 14 days following STEMI blunts the inflammatory response and appears to reduce the occurrence of HF events at 1 year. These results support the hypothesis that early and targeted modification of the inflammatory response in STEMI may be a viable strategy to improve patient outcomes. Adjudicated events at 1 year Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): National Heart Lung and Blood Institute (USA), American Heart Association (USA)

Supplemental Digital Content is Available in the Text., The NLRP3 inflammasome has been implicated in the development and progression of heart failure. The aim of this study was to determine the safety of an oral inhibitor of the NLRP3 inflammasome, dapansutrile (OLT1177), in patients with heart failure and reduced ejection fraction (HFrEF). This was a phase 1B, randomized, double-blind, dose escalation, single-center, repeat dose safety and pharmacodynamics study of dapansutrile in stable patients with HFrEF (New York Heart Association Class II–III). Subjects were randomized to treatment with dapansutrile for up to 14 days at a ratio of 4:1 into 1 of 3 sequential ascending dose cohorts (500, 1000, or 2000 mg) each including 10 patients. Subjects underwent clinical assessment, biomarker determination, transthoracic echocardiogram, and maximal cardiopulmonary exercise testing at baseline, day 14, and day 28 to ascertain changes in clinical status. Placebo cases (N = 2 per cohort) were used as a decoy to reduce bias and not for statistical comparisons. Thirty participants (20 men) were treated for 13 (12–14) days. No serious adverse events during the study were recorded. All clinical or laboratory parameters at day 14 compared with baseline suggested clinical stability without significant within-group differences in the dapansutrile-pooled group or the 3 dapansutrile cohorts. Improvements in left ventricular EF [from 31.5% (27.5–39) to 36.5% (27.5–45), P = 0.039] and in exercise time [from 570 (399.5–627) to 616 (446.5–688) seconds, P = 0.039] were seen in the dapansutrile 2000 mg cohort. Treatment with dapansutrile for 14 days was safe and well tolerated in patients with stable HFrEF.

Previous studies suggested that N-terminal pro-brain natriuretic peptide (NT-proBNP) level is a powerful independent predictor of death or heart failure (HF) when measured at admission in patients with chest pain or acute coronary syndrome. Little is known about the role of NT-proBNP level measured during a hospitalization for ST segment elevation myocardial infarction (STEMI) in predicting clinical outcomes. We evaluated the optimal NT-proBNP timing (admission, 72 hours, or delta [Δ] NT-proBNP [72 hours minus admission]) to predict 1-year new-onset HF in STEMI patients.We measured NT-proBNP levels at admission and 72 hours in 72 patients with STEMI. HF events were adjudicated and defined as hospitalization for HF or need for new initiation of a loop diuretic at 1-year follow-up. Values are presented as medians and interquartile range or frequencies (%) as appropriate. Cox regression analysis was used to determine predictors of adverse events. A receiver-operative-curve was constructed to identify the discriminative value and optimal cut-off points for NT-proBNP.Patients (age 56 [49-64] years, males 59 [82%]) were followed for a median duration of 365 [180-365] days. HF events were recorded in 9 (12.5%) patients. NT-proBNP values at admission, 72 hours, and ΔNT-proBNP were 89 (26-268) pg/mL, 452 (223-1064) pg/mL, and 283 (68-686) pg/mL, respectively. NT-proBNP at 72 hours and ΔNT-proBNP, but not admission NT-proBNP predicted new-onset HF events at follow-up (P=0.03, P=0.002 and P=0.89, respectively). The optimal area under the curve of 0.771 (95%, CI [0.630-0.912], P= 0.009) and cut-off value of 830 pg/mL (sensitivity 79%; specificity 76%) were found for NT-proBNP at 72 hours. The Kaplan-Meier survival curves for NT-proBNP at 72 hours dichotomized above and below this cut-off value, confirmed NT-proBNP at 72 hours830 pg/mL as predictive of HF events (log-rank statistic = 8.688, P=0.003).NT-proBNP level at 72 hours and ΔNT-proBNP (72 hours minus admission), but not at time of admission, predicted HF events in patients following STEMI.