Full-Time Cardiac Intensive Care Unit Staffing by Heart Failure Specialists and its Association with Mortality Rates.

BACKGROUND: Cardiac intensive care units (CICUs) serve medically complex patients with multiorgan dysfunction. Whether a CICU that is staffed full time by heart failure (HF) specialists is associated with decreased mortality is unclear. METHODS AND RESULTS: A retrospective review of consecutive CICU admissions from January 1, 2012, to December 31, 2016, was performed. In January 2014, the CICU changed from an open unit staffed by any cardiologist to a closed unit managed by HF specialists. Patients' baseline characteristics were determined, and a multivariate regression analysis was performed to ascertain mortality rates in the CICU. Baseline severity of illness was higher in the closed/HF specialist CICU model (P< 0.001). Death occurred in 101 of 1185 patients admitted to the CICU (8.5%) in the open-unit model and in 139 of 2163 patients (6.4%) admitted to the closed/HF specialist model (absolute risk reduction 2.1%, 95% confidence interval [CI] 0.1-4.0%; P = 0.01). The transition from an open to a closed/HF specialist model was associated with a lower overall CICU mortality rate (odds ratio [OR] 0.63; 95% CI 0.43-0.93). Prespecified interaction with a mechanical circulatory support device and unit model showed that treatment with such a device was associated with lower mortality rates in the closed/HF specialist model of a CICU (OR 0.6; 95% CI 0.18-0.78; P for interaction <0.01). CONCLUSION: Transition to a closed unit model staffed by a dedicated HF specialist is associated with lower CICU mortality rates.

Validation of the Khorana score in acute myeloid leukemia patients: a single-institution experience.

BACKGROUND: Although patients with acute myeloid leukemia (AML) were shown to have an increased risk of thrombosis, no thrombosis risk assessment scoring system has been developed for AML patients. The Khorana Risk Score (KRS), which has been widely used for thrombosis risk assessment in the clinical setting, was developed on the basis of solid tumor data and has not been validated among AML patients. This study aims to validate the use of the KRS as a thrombosis risk-scoring system among patients with AML. METHODS: Using data from H. Lee Moffitt Cancer Center and Research Institution's Total Cancer Care Research Study, we retrospectively identified patients who were histologically confirmed with AML from 2000 to 2018. Clinical and laboratory variables at the time of AML diagnosis were characterized and analyzed. The thrombotic event rate was estimated with the Kaplan-Meier method and compared using the log-rank test. RESULTS: A total of 867 AML patients were included in the analysis. The median age at AML diagnosis was 75 years (range, 51-96), and the majority were male (65%, n = 565). A total of 22% (n = 191), 51% (n = 445), 24% (n = 207), and 3% (n = 24) of patients had a KRS of 0, 1, 2, and 3, respectively. A total of 42 thrombotic events (3% [n = 6/191] with a KRS of 1; 5% [n = 23/445] with a KRS of 2; 6.3% [n = 13/207] with a KRS of 3) were observed, with a median follow-up of 3 months (range, 0.1-307). There was no statistical difference in the risk of thrombosis between these groups (P = .1949). CONCLUSIONS: Although there was an increased risk of thrombosis associated with a higher KRS among AML patients with a KRS of 1 to 3, the difference was not statistically significant. Furthermore, only a few patients were found to have a KRS > 3, and this was largely due to pancytopenia, which is commonly associated with AML. These results indicate the need for a better thrombotic risk-scoring system for AML patients.

Mitochondrial DNA Double-Strand Breaks in Oligodendrocytes Cause Demyelination, Axonal Injury, and CNS Inflammation.

Mitochondrial dysfunction has been implicated in the pathophysiology of neurodegenerative disorders, including multiple sclerosis (MS). To date, the investigation of mitochondrial dysfunction in MS has focused exclusively on neurons, with no studies exploring whether dysregulation of mitochondrial bioenergetics and/or genetics in oligodendrocytes might be associated with the etiopathogenesis of MS and other demyelinating syndromes. To address this question, we established a mouse model where mitochondrial DNA (mtDNA) double-strand breaks (DSBs) were specifically induced in myelinating oligodendrocytes (PLP:mtPstI mice) by expressing a mitochondrial-targeted endonuclease, mtPstI, starting at 3 weeks of age. In both female and male mice, DSBs of oligodendroglial mtDNA caused impairment of locomotor function, chronic demyelination, glial activation, and axonal degeneration, which became more severe with time of induction. In addition, after short transient induction of mtDNA DSBs, PLP:mtPstI mice showed an exacerbated response to experimental autoimmune encephalomyelitis. Together, our data demonstrate that mtDNA damage can cause primary oligodendropathy, which in turn triggers demyelination, proving PLP:mtPstI mice to be a useful tool to study the pathological consequences of mitochondrial dysfunction in oligodendrocytes. In addition, the demyelination and axonal loss displayed by PLP:mtPstI mice recapitulate some of the key features of chronic demyelinating syndromes, including progressive MS forms, which are not accurately reproduced in the models currently available. For this reason, the PLP:mtPstI mouse represents a unique and much needed platform for testing remyelinating therapies.SIGNIFICANCE STATEMENT In this study, we show that oligodendrocyte-specific mitochondrial DNA double-strand breaks in PLP:mtPstI mice cause oligodendrocyte death and demyelination associated with axonal damage and glial activation. Hence, PLP:mtPstI mice represent a unique tool to study the pathological consequences of mitochondrial dysfunction in oligodendrocytes, as well as an ideal platform to test remyelinating and neuroprotective agents.

Subacute Cardiac Tamponade in a COVID-19 Patient Despite Negative Testing.

COVID-19 infection has been documented to cause a wide range of symptoms including cardiac complications. We present a case of subacute cardiac tamponade in a patient infected with COVID-19 in the absence of respiratory symptoms; we also review the current literature on this rare sequela. Our patient is a 67-year-old man who presented to the hospital due to intermittent chest pain for three weeks. COVID-19 polymerase chain reaction (PCR) testing was negative two times. He had an outpatient echocardiogram that showed a moderate pericardial effusion about a week prior to the hospital presentation. On admission, a repeat echocardiogram showed a large pericardial effusion with tamponade physiology. Pericardiocentesis did not reveal a clear etiology of the hemorrhagic effusion but four days later, the patient was found to be positive for COVID-19 infection without any clear respiratory illness. Given the absence of other etiology and negative workup, cardiac tamponade was attributed to pericardial inflammation from this virus and our patient improved with colchicine and steroids. We, therefore, advise providers to consider COVID-19 as a cause of hemorrhagic, cryptogenic cardiac tamponade despite negative COVID-19 testing. We also review 42 additional reported cases of cardiac tamponade in patients infected with COVID-19. COVID-19 can cause cardiac tamponade even in the absence of pulmonary disease. This case and literature review highlight tamponade as a rare complication of COVID-19 and should be considered in the differential of any acute deterioration in this patient population.

Evaluation of a novel virtual care platform for remote monitoring of LVAD patients.

The aim of this study was to evaluate a novel virtual care platform created for use in Left Ventricular Assist Device (LVAD) patients. The platform included a daily log of LVAD parameters and medication adherence, two-way messaging with providers, and educational resources. To test the feasibility of this application, we recruited 25 patients between 2017 and 2019 and followed them for 6 months post discharge. Feedback concerning the platform was very positive with an average score of 4.5 ± 0.6 (out of 5) on usability and/or satisfaction and 8.1 ± 1.8 (out of 10) on likelihood to recommend the platform. In addition, our platform was well utilized with median (IQR) engagement rates of 87 (53,100)% at 30 days and 73 (49,95)% overall. We found that patients using the platform attended significantly less outpatient visits at the 6 month mark, however there was no difference in 30-day readmission rates compared to the overall LVAD cohort.

Determining the optimal duration for premature ventricular contraction monitoring.

BACKGROUND: Premature ventricular contractions (VPC) have hour-to-hour and day-to-day variation. High VPC burden correlates with cardiomyopathy. OBJECTIVE: To determine the optimal duration for ambulatory electrocardiogram monitoring for accurate assessment of VPC burden. METHODS: Our group performed a retrospective analysis on patch monitors used for any indication with overall VPC burden ≥5.0% between February 1, 2016, and February 1, 2020. We generated cumulative daily VPC averages for each day of wear and performed linear regression analysis between each cumulative daily average and overall burden. Patients were divided into groups based on low or high VPC frequency, and the analysis was repeated. Split-sample validation was used to internally validate the overall prediction model. RESULTS: A total of 116 patches representing 107 patients (mean age: 64.5; female: 48%) were analyzed. Mean overall VPC burden was 13.4% ± 7.5% (range: 5.0%-42.0%). Day 1 R2 was 60%, P < .001, and continued to increase to R2 88%, P < .001 at day 14. Median percent and absolute error decreased from 22.70% (interquartile range [IQR]: 9.73-34.39) and 2.58% (IQR: 1.24-4.59) at day 1 to 5.62% (IQR: 2.82-8.39) and 0.55% (IQR: 0.28-1.05) at day 14. Patients with higher overall VPC frequencies achieved a more rapid rise in R2 relative to those with lower frequencies. Split-sample validation supported the internal validity of our linear regression prediction model. CONCLUSION: Mobile telemetry for a period of ∼7 days accurately reflects overall VPC burden. Measurement of VPC burden for only 24-48 hours may not accurately reflect total burden. Monitoring for 2 weeks or longer adds little additional VPC information.