Use of Imaging-guided Decongestion for Reducing Heart Failure Readmission and Death in High-risk Patients: A Multi-site Randomized Trial of a Nurse-led Strategy at the Point of Care.

BACKGROUND: Nurse-led disease management programs (DMPs) decrease readmission after acute decompensated heart failure (HF). We sought whether readmissions could be further reduced by lung ultrasound (LUS)-guided decongestion before discharge and during DMP. METHODS AND RESULTS: Of 290 patients hospitalized with acute decompensated HF, 122 at high risk for readmission or mortality were randomized to receive usual care (UC) (n = 64) or UC plus intervention (DMP-Plus) (n = 58), comprising LUS-guided management before discharge and during at-home follow-up. Residual congestion was identified by ≥10 B-lines detected in 8 lung zones. The outcomes included a composite of readmission and/or mortality at 30 and 90 days, and 90-day HF readmission. Residual congestion was detected equally among the patient groups. The 30-day composite outcome occurred in 28% DMP-plus patients and 22% UC patients (odd ratio [OR], 1.36; 95% confidence interval [CI], 0.59-3.1; P = .5) and the 90-day HF readmission outcome occurred in 22% and 31%, respectively (odds ratio, 0.63; 95% CI, 0.28-1.43; P = .3). Residual congestion, identified at predischarge LUS examination in high-risk patients, was associated with early (<14-day) HF readmission (relative risk, 1.19; 95% CI, 1.06-1.32; P = .002) and multiple (≥2) readmissions over 90 days of follow-up (relative risk, 1.09; 95% CI, 1.01-1.16; P = .012), independent of demographics and comorbidities. CONCLUSIONS: Readmission in patients with incomplete decongestion before discharge occurs within the first 2 weeks. However, our DMP-plus strategy did not improve the primary outcome.

HeartMate 3 implantation with an emphasis on the biventricular configuration.

OBJECTIVES: Right ventricular failure following implantation of a durable left ventricular assist device (LVAD) is a major driver of mortality. Reported survival following biventricular (BiVAD) or total artificial heart (TAH) implantation remains substantially inferior to LVAD alone. We report our outcomes with LVAD and BiVAD HeartMate 3 (HM3). METHODS: Consecutive patients undergoing implantation of an HM3 LVAD between November 2014 and December 2021, at The Alfred, Australia were included in the study. Comparison was made between the BiVAD and LVAD alone groups. RESULTS: A total of 86 patients, 65 patients with LVAD alone and 21 in a BiVAD configuration underwent implantation. The median age of the LVAD and BiVAD groups was 56 years (Interquartile range 46-62) and 49 years (Interquartile range 37-55), respectively. By 4 years after implantation, 54% of LVAD patients and 43% of BiVAD patients had undergone cardiac transplantation. The incidence of stroke in the entire experience was 3.5% and pump thrombosis 5% (all in the RVAD). There were 14 deaths in the LVAD group and 1 in the BiVAD group. The actuarial survival for LVAD patients at 1 year was 85% and BiVAD patients at 1 year was 95%. CONCLUSIONS: The application of HM 3 BiVAD support in selected patients appears to offer a satisfactory solution to patients requiring biventricular support.

2024 Australia-New Zealand Expert Consensus Statement on Cardiac Amyloidosis.

Over the past 5 years, early diagnosis of and new treatments for cardiac amyloidosis (CA) have emerged that hold promise for early intervention. These include non-invasive diagnostic tests and disease modifying therapies. Recently, CA has been one of the first types of cardiomyopathy to be treated with gene editing techniques. Although these therapies are not yet widely available to patients in Australia and New Zealand, this may change in the near future. Given the rapid pace with which this field is evolving, it is important to view these advances within the Australian and New Zealand context. This Consensus Statement aims to update the Australian and New Zealand general physician and cardiologist with regards to the diagnosis, investigations, and management of CA.

Incidence and Predictors of Eosinophilic Myocardial Hypersensitivity in Patients Receiving Home Dobutamine.

ABSTRACT: We sought to examine incidence and predictors of eosinophilic myocardial hypersensitivity (EMH) in a cohort of patients in the home inotrope program of a quaternary cardiac transplant center. Patients on home inotropes with progression to heart transplantation or ventricular assist device (VAD) between January 2000 and May 2020 were included. EMH was diagnosed by the presence of an interstitial predominate eosinophilic infiltrate within the myocardium by experienced cardiac pathologists. From a cohort of 74 patients, 58% (43) were on dobutamine and 42% (31) were on milrinone. Dobutamine was associated with EMH incidence of 14% (6/43), with zero cases in the milrinone cohort. Mean age was 52 ± 12 years, 22% were female. More than half (62%) were nonischemic dilated cardiomyopathies, the remainder were ischemic cardiomyopathy. Dobutamine dose [250 (200-282) vs. 225 (200-291) µg/min] and duration of therapy [41 (23-79) vs. 53 (24-91) days] was similar between those with and without EMH. Median change in eosinophil count was 0.31 × 10 9 /L in the EMH group compared with only 0.03 × 10 9 /L in the non-EMH cohort, P = 0.02. Increase in peripheral eosinophil count of >0.20 × 10 9 /L demonstrated good discrimination between those with and without EMH, c-statistic 0.83 (95% CI 0.66-1.0). Heart failure hospitalization occurred in 83% of the EMH group versus 59% in the non-EMH group, P = 0.26. Requirement for VAD was significantly higher in the EMH group (83% vs. 41%, P = 0.05). In conclusion, EMH occurred in 14% of patients receiving home dobutamine. Rising eosinophil count should prompt physicians to consider EMH and switch to milrinone to avoid possible escalation to VAD.

Levosimendan and Continuous Outpatient Support With Inotropes in Patients With Advanced Heart Failure: A Single-Centre Descriptive Study.

ABSTRACT: To describe the use of levosimendan in a quaternary referral center with a dedicated heart failure service and compare its efficacy and safety to continuous outpatient support with inotropes (COSI) among patients with advanced heart failure (AHF) who require bridge-to-decision (BTD) or bridge-to-transplant (BTT) therapy. This study was a retrospective, single-center, descriptive study of patients with AHF who received either a single levosimendan infusion or COSI between 2018 and 2021. A total of 23 patients received a levosimendan infusion, and 14 were started on COSI. Three indications for levosimendan were identified: (1) to facilitate weaning of continuous inotropes, (2) to augment diuresis in cardiorenal syndrome, and (3) as first-line therapy for cardiogenic shock in selected patients. Eighty-three percent (19 of 23) of patients who received levosimendan survived to discharge, and there were few clinically significant adverse events. Overall survival at 12 months among patients who received levosimendan was 74%. No statistically significant difference in survival was observed at 12 months (P = 0.68) or beyond (P = 0.63) between patients who received levosimendan and were discharged with a plan for BTD or BTT and those who received COSI. Levosimendan is a safe and effective short-term therapy in AHF and offers comparable long-term survival to COSI in patients who require BTD or BTT therapy.

Reduction in mortality from implantable cardioverter-defibrillators in non-ischaemic cardiomyopathy patients is dependent on the presence of left ventricular scar.

Aims: In patients with non-ischaemic cardiomyopathy (NICM), the mortality benefit of a primary prevention implantable cardioverter-defibrillator (ICD) has been challenged. Left ventricular (LV) scar identified by cardiac magnetic resonance (CMR) imaging is associated with a high risk of malignant arrhythmia in NICM. We aimed to determine the impact of LV scar on the mortality benefit from a primary prevention ICD in NICM. Methods and results: We recruited 452 consecutive heart failure patients [New York Heart Association (NYHA) Class II/III] with NICM and LV ejection fraction ≤35% from a state-wide CMR service. All patients fulfilled European Society of Cardiology guidelines for primary prevention ICD implantation; however, the decision to implant was at the treating physician's discretion. Baseline clinical and CMR data were recorded prospectively and heart failure mortality risk (MAGGIC score) was calculated. The primary study outcome measurement was all-cause mortality based on presence or absence of ICD, stratified by LV scar. Median follow-up was 37.9 months and there was no difference in MAGGIC score between those who did and did not receive a primary prevention ICD (19.30 ± 5.46 vs. 18.90 ± 5.67, P = 0.50). In patients without LV scar, ICD implantation was not associated with improved mortality [hazard ratio (HR) = 1.22, 95% confidence interval (CI): 0.53-2.78, P = 0.64]. In patients with LV scar, ICD implantation was independently associated with reduced mortality (HR = 0.45, 95% CI: 0.26-0.77, P = 0.003). Conclusions: In patients with NICM, primary prevention ICD implantation is only associated with reduced mortality in patients with LV scar. This may enable more effective selection of NICM patients for ICD implantation compared with current guidelines.

Diffuse Ventricular Fibrosis on Cardiac Magnetic Resonance Imaging Associates With Ventricular Tachycardia in Patients With Hypertrophic Cardiomyopathy.

INTRODUCTION: Non-sustained ventricular tachycardia (NSVT) is a risk factor for sudden cardiac death (SCD) in patients with hypertrophic cardiomyopathy (HCM). We aimed to assess whether diffuse ventricular fibrosis on cardiac magnetic resonance (CMR) imaging could be a surrogate marker for ventricular arrhythmias in patients with HCM. METHODS: A total of 100 patients with HCM (mean age 51 ± 13 years, septal wall thickness 20 ± 5 mm) underwent CMR with a 1.5 T scanner to determine the presence of ventricular late gadolinium enhancement (LGE) for focal fibrosis, and post-contrast T1 mapping for diffuse ventricular fibrosis. The presence of NSVT was determined by Holter monitoring and a subset of high risk patients received an implantable cardioverter-defibrillator (ICD). RESULTS: NSVT was detected in 23 of 100 patients with HCM. Focal ventricular fibrosis (by LGE) was observed in 87%, with no significant difference between patients with (96%) or without NSVT (86%, P = 0.19). However, LGE mass was greater in patients with (16.5 ± 19.1 g) versus without NSVT (7.6 ± 10.2 g, P < 0.01). NSVT was associated with a significant reduction in ventricular T1 relaxation time (422 ± 54 milliseconds) versus patients without NSVT (512 ± 115 milliseconds; P < 0.001). There was significant reduction in ventricular T1 relaxation time in patients with (430 ± 48 milliseconds) versus without aborted SCD (495 ± 113 milliseconds; P = 0.01) over a mean follow-up of 40 ± 10 months. On multivariate analysis post-contrast ventricular T1 relaxation time and septal wall thickness were the only predictors of NSVT. CONCLUSION: Post-contrast T1 relaxation time on CMR is associated with ventricular arrhythmias in patients with HCM. Diffuse ventricular fibrosis may be an important marker of arrhythmic risk in patients with HCM.

Asymptomatic myocarditis during clozapine re-titration, in a patient who had previously been stable on clozapine for 10 years.

OBJECTIVE: We present a case of confirmed clozapine-induced myocarditis in a patient who was not naïve to the drug. METHOD: This patient, who had been stable on clozapine for 10 years, relapsed following self-cessation. Asymptomatic throughout inpatient re-titration, serum cardiac enzymes were nonetheless routinely taken. RESULTS: Occult myocarditis was only discovered due to an elevated Troponin I, and was confirmed by cardiac imaging. CONCLUSIONS: Once thought to be the preserve of initial exposure to the medication, clozapine-induced myocarditis can occur at any re-titration point if the immunological milieu permits. We therefore recommend routine monitoring of serum cardiac enzymes with all patients undergoing titration of clozapine, regardless of whether they have previously been stable on the drug.

Hypothermic oxygenated perfusion (HOPE) safely and effectively extends acceptable donor heart preservation times: Results of the Australian and New Zealand trial.

BACKGROUND: Cold static storage preservation of donor hearts for periods longer than 4 hours increases the risk of primary graft dysfunction (PGD). The aim of the study was to determine if hypothermic oxygenated perfusion (HOPE) could safely prolong the preservation time of donor hearts. METHODS: We conducted a nonrandomized, single arm, multicenter investigation of the effect of HOPE using the XVIVO Heart Preservation System on donor hearts with a projected preservation time of 6 to 8 hours on 30-day recipient survival and allograft function post-transplant. Each center completed 1 or 2 short preservation time followed by long preservation time cases. PGD was classified as occurring in the first 24 hours after transplantation or secondary graft dysfunction (SGD) occurring at any time with a clearly defined cause. Trial survival was compared with a comparator group based on data from the International Society of Heart and Lung Transplantation (ISHLT) Registry. RESULTS: We performed heart transplants using 7 short and 29 long preservation time donor hearts placed on the HOPE system. The mean preservation time for the long preservation time cases was 414 minutes, the longest being 8 hours and 47 minutes. There was 100% survival at 30 days. One long preservation time recipient developed PGD, and 1 developed SGD. One short preservation time patient developed SGD. Thirty day survival was superior to the ISHLT comparator group despite substantially longer preservation times in the trial patients. CONCLUSIONS: HOPE provides effective preservation out to preservation times of nearly 9 hours allowing retrieval from remote geographic locations.

Recurrent myocarditis--an important mimic of ischaemic myocardial infarction.

Patients presenting with a syndrome of chest pain, elevated cardiac enzyme levels with or without electrocardiogram changes are a common diagnostic and management problem in cardiology. Most commonly, this is due to ischaemic myocardial infarction secondary to coronary artery disease. However, when coronary angiography does not demonstrate any obstructive coronary artery lesion, the diagnosis of myocarditis should be considered. Cardiac magnetic resonance imaging is helpful towards making this diagnosis. Here, we describe the first reported Australian cases of recurrent myocarditis presenting with ischaemic chest pain and elevated cardiac enzyme levels. These cases serve as an important reminder to clinicians that myocarditis is an important mimic of ischaemic myocardial infarction.

Diffuse myocardial fibrosis in hypertrophic cardiomyopathy can be identified by cardiovascular magnetic resonance, and is associated with left ventricular diastolic dysfunction.

BACKGROUND: The presence of myocardial fibrosis is associated with worse clinical outcomes in hypertrophic cardiomyopathy (HCM). Cardiovascular magnetic resonance (CMR) with late gadolinium enhancement (LGE) sequences can detect regional, but not diffuse myocardial fibrosis. Post-contrast T(1) mapping is an emerging CMR technique that may enable the non-invasive evaluation of diffuse myocardial fibrosis in HCM. The purpose of this study was to non-invasively detect and quantify diffuse myocardial fibrosis in HCM with CMR and examine its relationship to diastolic performance. METHODS: We performed CMR on 76 patients - 51 with asymmetric septal hypertrophy due to HCM and 25 healthy controls. Left ventricular (LV) morphology, function and distribution of regional myocardial fibrosis were evaluated with cine imaging and LGE. A CMR T(1) mapping sequence determined the post-contrast myocardial T(1) time as an index of diffuse myocardial fibrosis. Diastolic function was assessed by transthoracic echocardiography. RESULTS: Regional myocardial fibrosis was observed in 84% of the HCM group. Post-contrast myocardial T(1) time was significantly shorter in patients with HCM compared to controls, consistent with diffuse myocardial fibrosis (498 ± 80 ms vs. 561 ± 47 ms, p < 0.001). In HCM patients, post-contrast myocardial T(1) time correlated with mean E/e' (r = -0.48, p < 0.001). CONCLUSIONS: Patients with HCM have shorter post-contrast myocardial T(1) times, consistent with diffuse myocardial fibrosis, which correlate with estimated LV filling pressure, suggesting a mechanistic link between diffuse myocardial fibrosis and abnormal diastolic function in HCM.

Improvement in functional capacity with spironolactone masks the treatment effect on exercise blood pressure.

OBJECTIVES: A hypertensive response to submaximal exercise is associated with cardiovascular disease but this relationship is influenced by functional capacity. Spironolactone improves functional capacity, which could mask treatment effects on exercise blood pressure. This study sought to examine this hypothesis. DESIGN: Retrospective analysis of a randomized clinical trial. METHODS: 102 participants (54 ±â€¯9 years; 52% male) with a hypertensive response to maximal exercise (systolic BP ≥210 mm Hg men; ≥190 mm Hg women) were randomized to 3-month spironolactone 25 mg daily (n = 53) or placebo (n = 49). Submaximal exercise blood pressure was measured during low-intensity cycling (50, 60 or 70% age-predicted maximal heart rate). Functional capacity was measured as maximal oxygen capacity obtained during a maximal treadmill exercise test, and (resting) aortic stiffness by carotid-to-femoral pulse wave velocity. RESULTS: Spironolactone improved submaximal exercise systolic blood pressure vs. placebo (-4 ±â€¯16 vs. 2 ±â€¯15 mm Hg, p = 0.045, Cohen's d = 0.42), and had a small (but non-statistically significant) improvement in functional capacity (0.64 ±â€¯5.10 vs. -1.43 ±â€¯5.04 ml/kg/min, p = 0.06, Cohen's d = 0.4). When treatment effects were expressed as the change in submaximal exercise systolic blood pressure relative to the change in functional capacity, a larger effect size was observed (-0.3 ±â€¯1.1 vs. 0.3 ±â€¯1.1 mm Hg/ml·kg·min-1, p = 0.01, Cohen's d = 0.58), but was not explained by improved aortic stiffness. CONCLUSIONS: Spironolactone reduces submaximal exercise blood pressure, but this treatment effect may be hidden by improved functional capacity and a non-fixed workload. This highlights the most clinically relevant exercise blood pressure is at a low intensity and fixed workload where the influence of fitness on exercise blood pressure is removed, and the effects of therapy can be appreciated.

Type-2 Diabetes and the Clinical Importance of Exaggerated Exercise Blood Pressure.

BACKGROUND: Exaggerated exercise blood pressure (EEBP) during clinical exercise testing is associated with poor blood pressure (BP) control and cardiovascular disease (CVD). Type-2 diabetes (T2DM) is thought to be associated with increased prevalence of EEBP, but this has never been definitively determined and was the aim of this study. METHODS: Clinical exercise test records were analyzed from 13 268 people (aged 53±13 years, 59% male) who completed the Bruce treadmill protocol (stages 1-4, and peak) at 4 Australian public hospitals. Records (including BP) were linked to administrative health datasets (hospital and emergency admissions) to define clinical characteristics and classify T2DM (n=1199) versus no T2DM (n=12 069). EEBP was defined as systolic BP ≥90th percentile at each test stage. Exercise BP was regressed on T2DM history and adjusted for CVD and risk factors. RESULTS: Prevalence of EEBP (age, sex, preexercise BP, hypertension history, CVD history and aerobic capacity adjusted) was 12% to 51% greater in T2DM versus no T2DM (prevalence ratio [95% CI], stage 1, 1.12 [1.02-1.24]; stage 2, 1.51 [1.41-1.61]; stage 3, 1.25 [1.10-1.42]; peak, 1.18 [1.09-1.29]). At stages 1 to 3, 8.6% to 15.8% (4.8%-9.7% T2DM versus 3.5% to 6.1% no-T2DM) of people with 'normal' preexercise BP (<140/90 mm Hg) were identified with EEBP. Exercise systolic BP relative to aerobic capacity (stages 1-4 and peak) was higher in T2DM with adjustment for all CVD risk factors. CONCLUSIONS: People with T2DM have higher prevalence of EEBP and exercise systolic BP independent of CVD and many of its known risk factors. Clinicians supervising exercise testing should be alerted to increased likelihood of EEBP and thus poor BP control warranting follow-up care in people with T2DM.

Masked hypertension is "unmasked" by low-intensity exercise blood pressure.

PURPOSE: Masked hypertension (MH) independently predicts mortality but cannot be diagnosed from clinic blood pressure (BP) taken under resting conditions. We sought to determine if MH could be identified from BP taken during a single bout of low-intensity exercise. METHODS: BP was recorded at rest and during brief low-level cycling exercise (60-70% of age-predicted maximal heart rate) in 75 untreated subjects with a hypertensive response to exercise (aged 54 ± 9 years). All subjects underwent 24-h ambulatory BP monitoring (ABPM) and MH was defined as clinic BP < 140/90 mmHg and ABPM BP ≥ 130/80 mmHg. RESULTS: There were 42 (56%) patients with MH, and at rest systolic (SBP) was higher in subjects with MH compared with those without MH (127 ± 9 vs 120 ± 9 mmHg; p < 0.05). During exercise, MH subjects had significantly higher SBP (188 ± 22 vs 168 ± 15 mmHg; p < 0.05), with a greater change from baseline (61 ± 21 vs 48 ± 15 mmHg; p < 0.05). Low-level exercise SBP was independently associated with MH, and if ≥ 175 mmHg, identified MH with 74% sensitivity and 67% specificity (p < 0.001). CONCLUSION: MH can be identified in untreated individuals from low-intensity exercise SBP. Further research on the diagnostic value of BP during early phases of exercise stress testing is needed.

Cognitive impairment as a determinant of response to management plans after heart failure admission.

AIMS: Cognitive impairment (CI) is highly prevalent in heart failure (HF), and increases patients' risks of readmission. This study sought to determine whether the presence and degree of CI could identify patients most likely to benefit from a HF disease management programme (DMP) to reduce readmissions. METHODS AND RESULTS: A total of 1152 consecutive Australian patients admitted with HF (2014-2017) were prospectively followed up for 12 months. Of these, 324 patients who received DMP (1-month duration, including post-discharge home visits, medication reconciliation, exercise guidance and early clinical review) were matched (1:2 ratio) with 648 usual care patients. Cognitive function was assessed either on the day of or one day before discharge using the Montreal Cognitive Assessment (MoCA). Outcomes included readmission or death at 1, 3 and 12 months, and days at home within 12 months of discharge. Poorer cognitive function was associated with all adverse outcomes. Compared with usual care, DMP was associated with lower odds of 30-day [odds ratio (OR) 0.60, 95% confidence interval 0.40, 0.91] and 90-day (OR 0.53, 95% confidence interval 0.36, 0.77) readmission or death, and with 19 more days at home within 12 months, independent of HF therapy. The effect sizes of these associations were greater for patients with diminished cognition than those with normal cognition (interaction P = 0.036), and might have been more pronounced among those with mild CI compared with those with more severe CI (MoCA score 17-22; OR 0.42, 95% confidence interval 0.21, 0.87) at 30 days (OR 0.31, 95% confidence interval 0.16, 0.60 at 90 days). Patients with normal cognition had fewer events, irrespective of DMP. CONCLUSIONS: Cognitive function may determine how HF patients respond to a DMP. Cognitive screening before implementation of a DMP may allow personalized plans for patients with different levels of cognitive function.

The results of a single-center experience with HeartMate 3 in a biventricular configuration.

BACKGROUND: Right ventricular (RV) failure after left ventricular assist device (VAD) implantation is a difficult problem. One solution is the implantation of continuous-flow VADs in a biventricular configuration. Disappointing survival and a concerning incidence of right-sided pump thrombosis have been previously reported. METHODS: From May 2017 to April 2020, a total of 12 patients underwent implantation of HeartMate 3 (HM3) biventricular VADs (BiVADs) as a bridge to cardiac transplantation. The right-sided pump was implanted in the right atrium in all cases. Adverse events and patient outcomes were determined. RESULTS: Patients were male, and the mean age was 44 years. The etiology was dilated cardiomyopathy (6 patients), sarcoid heart disease (2 patients), ischemic cardiomyopathy (1 patient), anthracycline cardiomyopathy (1 patient), non-compaction cardiomyopathy (1 patient), and arrhythmogenic RV cardiomyopathy with biventricular involvement (1 patient). There was 1 death from multisystem failure. There were 3 episodes of right VAD thrombus (thrombosis or clot ingestion); 1 managed medically, 1 recognized intraoperatively treated with clot retrieval, and 1 requiring pump exchange. There were 3 driveline infections. At 18 months after the procedure, 5 patients (41.7%) had undergone cardiac transplantation, 5 patients (41.7%) were alive and on biventricular support, 1 patient had died (8.3%), and 1 patient had VAD explantation for myocardial recovery (8.3%). Actuarial survival at 18 months was 91.7%. CONCLUSIONS: In this small study, HM3 BiVAD in these critically ill patients was used with low mortality. This suggests that the timely deployment of biventricular support with HM3 can be associated with favorable outcomes.

Excellent suppression of physiological myocardial FDG activity in patients with cardiac sarcoidosis.

INTRODUCTION: Suppression of physiological myocardial FDG activity is vital in patients undergoing PET/CT for assessment of known or suspected cardiac sarcoidosis. This study aims to evaluate the efficacy of physiological myocardial FDG suppression following a protocol change to a 24-h high fat very low carbohydrate (HFVLC) diet and prolonged fast. METHODS: A retrospective review of patients undergoing FDG PET/CT for the evaluation of cardiac sarcoidosis was performed. Prior to June-2018, patients were prepared with a single very high-fat low carbohydrate meal followed by a 12-18 h fast (group 1). After June-2018, a protocol change was initiated with patients prepared with a HFVLC diet for 24-h followed by a 12-18 h fast (group 2). Focal myocardial activity was classified as positive, absent activity as negative and diffuse/focal on diffuse activity as indeterminate. RESULTS: A total of 94 FDG PET/CT scans were included with 46 scans in group 1 and 48 scans in group 2. Studies were classified as positive, negative or indeterminate in 25 (54%), 7 (15%) and 14 (30%) scans in group 1 and in 13 (27%), 33 (69%) and 2 (4%) scans in group 2, respectively. In scans classified as negative, myocardial FDG activity was less than mediastinal blood pool activity in 5/7 (71%) scans in group 1 and 33/33 (100%) scans in group 2. CONCLUSION: Excellent myocardial FDG suppression can be achieved using a 24-h HFVLC diet and prolonged fast, resulting in a very low indeterminate scan rate in patients with known or suspected cardiac sarcoidosis.

Bariatric Surgery in Patients with Severe Heart Failure.

PURPOSE: Obesity and cardiac failure are globally endemic and increasingly intersecting. Bariatric surgery may improve cardiac function and act as a bridge-to-transplantation. We aim to identify effects of bariatric surgery on severe heart failure patients and ascertain its role regarding cardiac transplantation. MATERIALS AND METHODS: A retrospective study of a prospectively collected database identified heart failure patients who underwent bariatric surgery between 1 January 2008 and 31 December 2017. Patients were followed up 12 months post-operatively. Cardiac investigations, functional capacity, cardiac transplant candidacy, morbidity and length of stay were recorded. RESULTS: Twenty-one patients (15 males, 6 females), mean age 48.7 ± 10, BMI 46.2 kg/m2 (37.7-85.3) underwent surgery (gastric band (18), sleeve gastrectomy (2), biliopancreatic diversion (1)). There were no loss to follow-up. There was significant weight loss of 26.0 kg (5.0-78.5, p < 0.001), significant improvement of left ventricular ejection fraction (LVEF) (10.0 ± 11.9%, p < 0.001) and significant reduction of 0.5 New York Heart Association (NYHA) classification (0-2, p < 0.001). Multivariate models delineated the absence of atrial fibrillation and pre-operative BMI < 49 kg/m2 as significant predictors (adjusted R-square 69%) for improvement of LVEF. Mean length of stay was 3.6 days and in-hospital morbidity rate was 42.9%. One patient subsequently underwent a heart transplant, and two patients were removed from the waitlist due to clinical improvements. CONCLUSION: Bariatric surgery is safe and highly effective in obese patients with severe heart failure with substantial improvements in cardiac function and symptoms. A threshold pre-operative BMI of 49 kg/m2 and absence of atrial fibrillation may be significant predictors for improvement in cardiac function. There is a role for bariatric surgery to act as a bridge-to-transplantation or even ameliorate this requirement.