The Value of Fetuin-A as a Predictor to Identify Takotsubo Patients at Risk of Cardiovascular Events

Introduction: Takotsubo cardiomyopathy (TTC) remains a life-threatening disease with the risk of decompensated heart failure and arrhythmias. Valid markers for the prediction of outcome are unavailable. The novel biomarkers fetuin-A, matrix metalloproteinases-2 (MMP-2), myeloperoxidase (MPO), Syndecan-1 and CD40-L show promising results for risk stratification of cardiovascular patients. Nevertheless, clinical implementation has not been investigated in TTC patients. Methods: To investigate this issue, we evaluated clinical complications in 51 patients hospitalized for TTC and measured the serum levels of fetuin-A, MPO, MMP-2, Syndecan-1 and CD40-L within 24 h after admission. Results: Serum levels of Fetuin-A correlated inversely with the risk of cardiac decompensation and all cause complications within the acute phase of TTC. Fetuin-A levels over 190.1 µg/mL (AUC: 0.738, sensitivity 87.5%, specificity: 52.6%) indicate an acute phase of TTC without cardiac decompensation. Despite lower fetuin-A levels in patients with all cause complications, the combined endpoint remained slightly unmet (p = 0.058, AUC: 0.655). Patients with fetuin-A levels over 213.3 µg/mL are at risk of experiencing hemodynamic relevant rhythm disorders (AUC: 0.794; sensitivity: 75.0%, specificity: 79.1%). Other biomarkers failed to reveal a prognostic impact. Pro-BNP and hs troponin levels at admission did not predict adverse cardiac events. Conclusion: Fetuin-A is a promising marker in our study and could be of benefit for the prediction of short-term adverse cardiac events in TTC patients. Therefore, fetuin-A might be of value to evaluate an individual’s risk for complications within the acute phase of TTC and to individually choose the time of intensive care and hospitalization.

Management of spine fractures in ankylosing spondylitis and diffuse idiopathic skeletal hyperostosis: a challenge

OBJECTIVE Ankylosing spinal disorders (ASDs) such as ankylosing spondylitis (AS) and diffuse idiopathic skeletal hyperostosis (DISH) are complex diseases regarding diagnostics, treatment, and patient outcome, especially in trauma. Originating from rigid biomechanics and low bone quality in considerably comorbid patients, serious spinal injury requires thorough and immediate imaging and is frequently missed. The aim of this study was to evaluate patient characteristics as well as procedures in patients with ASD in order to identify the major particularities of treatment. METHODS A total of 60 patients aged 78.5 ± 8.9 years were retrospectively included. Preoperative imaging as well as surgical treatment procedures and postoperative patient outcome were analyzed, including 30-day readmissions. RESULTS CT imaging of the entire spine was performed within 24 hours after the initial trauma in 73.3% of patients. A delay in diagnostics (> 24 hours) occurred in 41.7% of patients transferred from primary care centers. At admission, 25.0% of patients had fracture-related neurological deficits (American Spinal Injury Association [ASIA] grades A and B in 4 patients, and ASIA grades C and D in 11 patients). A spinal epidural hematoma was found in 21.2% of patients and was symptomatic in 72.7% of those patients. Of the patients with fracture-related neurological deficits, 93.3% were operated on within 48 hours from symptom onset. One patient (1.7%) developed neurological deficits from diagnosis to surgery. Postoperatively, 18.3% of patients had surgical complications, and 76.7% of patients developed further medical issues, with pneumonia (38.3%), pulmonary decompensation (25.0%), and cardiac decompensation (20.0%) being the leading causes. The 30-day mortality rate was high at 10.0%. CONCLUSIONS Treatment of patients with ASDs is complex. While surgical outcome is usually good, the multimorbid nature of these patients results in a high rate of major medical complications. If an ankylosing disease is suspected, MRI of the entire spine is mandatory. Upon diagnosis, treatment should be performed in centers capable of managing all aspects of the regular complications these patients will develop.

Autoinflammation leading to autoimmunity in adult-onset Still’s disease: more than simple coincidence?

Background Adult-onset Still’s disease (AOSD) should be considered in the differential diagnosis of patients with endocarditis, with or without a cardiac decompensation. Case presentation We report the case of a 68-year-old Caucasian male diagnosed with AOSD after an initial acute manifestation of endocarditis with severe aortic acute manifestation of endocarditis with severe aortic insufficiency. The histological findings revealed Libman–Sacks endocarditis. He was treated with the IL-1 receptor inhibitor anakinra. Two years later the patient developed a symptomatic dilated cardiomyopathy with reduced ejection fraction (23.5%) and functional anti-beta-1-adrenergic receptor antibodies, which was initially treated with plasmapheresis; anakinra was maintained. While his AOSD symptoms responded well, our patient presented with recurrent arthritis in multiple joints, dual-energy CT showed urate deposition compatible with a gouty arthropathy. Over 7 years, he presented with recurrent episodes of arthritis and the adjustment of dosages of colchicine and febuxostat was needed. In 2018, our patient died due to a deterioration of his underlying cardiac disease. Conclusions Only two cases with initial endocarditis prior to AOSD diagnosis have been published, and we are not aware of any other cases reporting -β1AR-Ab development with DCM and gout in the setting of AOSD treated with anakinra.

Surgical management of extensive aortic root endocarditis with ventricular septal rupture: A case report

A 79-year-old man was referred for severe cardiac decompensation. Chest radiography showed severe pulmonary edema, and transesophageal echocardiography revealed a large quantity of vegetation on all aortic valve leaflets with severe aortic valve regurgitation, heterogeneous cavities adjacent to the aortic annulus, and ventricular septal rupture. We performed thorough and extensive debridement of the aortic root; including the infected ventricular septum, reconstructed the ventricular septum and aortic root using autologous and bovine pericardial patches; and placed a bioprosthetic stented valve. The patient was discharged without any complications, and without recurrence of the endocarditis in the four years post-surgery.

Autoinflammation Leading to Autoimmunity in Adult Onset Still’s Disease, More Than Simple Coincidence?

Background: Adult onset Still’s disease (AOSD) should be considered in the differential diagnosis of patients with endocarditis, with or without a cardiac decompensation. Case presentation: We report the case of a 68-year-old Caucasian male diagnosed with AOSD after an initial acute manifestation of endocarditis with severe aortic acute manifestation of endocarditis with severe aortic insufficiency. The histological findings revealed Libman-Sacks endocarditis. He was treated with the IL-1 receptor inhibitor anakinra. Two years later the patient developed a symptomatic dilated cardiomyopathy with reduced ejection fraction (23.5%) and functional anti-beta-1-adrenergic receptor antibodies, which was initially treated with plasmapheresis; anakinra was maintained. While his AOSD symptoms responded well, our patient presented with recurrent arthritis in multiple joints, dual energy-CT showed urate deposition compatible with a gouty arthropathy. Over seven years, he presented with recurrent episodes of arthritis and the adjustment of dosages of colchicine and febuxostat was needed. In 2018, our patient died due to a deterioration of his underlying cardiac disease. Conclusions: Only two cases with initial endocarditis prior to AOSD diagnosis have been published and we are not aware of any other cases reporting -β1AR-Ab development with DCM and gout in the setting of AOSD treated with anakinra.

Trying to Survive A Serious Heart Condition in Time of COVID-19

The world has suffered over the past year under COVID-19. Unfortunately, people still are getting sick from other, also severe, diseases. Although the COVID-19 infection is present, patients need treatment for other life-threatening conditions. We present the case of a 36-year-old patient with severe infective endocarditis with a large abscess of the aortic root, who also is COVID-19 positive. Definitive diagnostics and treatment were avoided due to COVID-19 infection. In the end, emergent surgery was indicated due to acute cardiac decompensation and the development of heart failure symptoms, and the patient recovered uneventfully after surgery.

Nicotinamide for the treatment of heart failure with preserved ejection fraction

Heart failure with preserved ejection fraction (HFpEF) is a highly prevalent and intractable form of cardiac decompensation commonly associated with diastolic dysfunction. Here, we show that diastolic dysfunction in patients with HFpEF is associated with a cardiac deficit in nicotinamide adenine dinucleotide (NAD+). Elevating NAD+ by oral supplementation of its precursor, nicotinamide, improved diastolic dysfunction induced by aging (in 2-year-old C57BL/6J mice), hypertension (in Dahl salt-sensitive rats), or cardiometabolic syndrome (in ZSF1 obese rats). This effect was mediated partly through alleviated systemic comorbidities and enhanced myocardial bioenergetics. Simultaneously, nicotinamide directly improved cardiomyocyte passive stiffness and calcium-dependent active relaxation through increased deacetylation of titin and the sarcoplasmic reticulum calcium adenosine triphosphatase 2a, respectively. In a long-term human cohort study, high dietary intake of naturally occurring NAD+ precursors was associated with lower blood pressure and reduced risk of cardiac mortality. Collectively, these results suggest NAD+ precursors, and especially nicotinamide, as potential therapeutic agents to treat diastolic dysfunction and HFpEF in humans.

Trajectories of Left Ventricular Ejection Fraction After Acute Decompensation for Systolic Heart Failure: Concomitant Echocardiographic and Systemic Changes, Predictors, and Impact on Clinical Outcomes

Background Prospective longitudinal follow‐up of left ventricular ejection fraction (LVEF) trajectories after acute cardiac decompensation of heart failure is lacking. We investigated changes in LVEF and covariates at 6‐months' follow‐up in patients with a predischarge LVEF ≤40%, and determined predictors and prognostic implications of LVEF changes through 18‐months' follow‐up. Methods and Results Interdisciplinary Network Heart Failure program participants (n=633) were categorized into subgroups based on LVEF at 6‐months' follow‐up: normalized LVEF (>50%; heart failure with normalized ejection fraction, n=147); midrange LVEF (41%–50%; heart failure with midrange ejection fraction, n=195), or persistently reduced LVEF (≤40%; heart failure with persistently reduced LVEF , n=291). All received guideline‐directed medical therapies. At 6‐months' follow‐up, compared with patients with heart failure with persistently reduced LVEF, heart failure with normalized LVEF or heart failure with midrange LVEF subgroups showed greater reductions in LV end‐diastolic/end‐systolic diameters (both P <0.001), and left atrial systolic diameter ( P =0.002), more increased septal/posterior end‐diastolic wall‐thickness (both P <0.001), and significantly greater improvement in diastolic function, biomarkers, symptoms, and health status. Heart failure duration <1 year, female sex, higher predischarge blood pressure, and baseline LVEF were independent predictors of LVEF improvement. Mortality and event‐free survival rates were lower in patients with heart failure with normalized LVEF ( P =0.002). Overall, LVEF increased further at 18‐months' follow‐up ( P <0.001), while LV end‐diastolic diameter decreased ( P =0.048). However, LVEF worsened ( P =0.002) and LV end‐diastolic diameter increased ( P =0.047) in patients with heart failure with normalized LVEF hospitalized between 6‐months' follow‐up and 18‐months' follow‐up. Conclusions Six‐month survivors of acute cardiac decompensation for systolic heart failure showed variable LVEF trajectories, with >50% showing improvements by ≥1 LVEF category. LVEF changes correlated with various parameters, suggesting multilevel reverse remodeling, were predictable from several baseline characteristics, and were associated with clinical outcomes at 18‐months' follow‐up. Repeat hospitalizations were associated with attenuation of reverse remodeling. Registration URL: https://www.controlled‐trials.com ; Unique identifier: ISRCTN23325295.