Correlates of 90-Day Mortality Among People Who Do and Do Not Inject Drugs With Infective Endocarditis in Seattle, Washington.

Background: Infective endocarditis (IE) remains highly morbid, but few studies have evaluated factors associated with IE mortality. We examined correlates of 90-day mortality among people who inject drugs (PWID) and people who do not inject drugs (non-PWID). Methods: We queried the electronic medical record for cases of IE among adults ≥18 years of age at 2 academic medical centers in Seattle, Washington, from 1 January 2014 to 31 July 2019. Cases were reviewed to confirm a diagnosis of IE and drug use status. Deaths were confirmed through the Washington State death index. Descriptive statistics were used to characterize IE in PWID and non-PWID. Kaplan-Meier log-rank tests and Cox proportional hazard models were used to assess correlates of 90-day mortality. Results: We identified 507 patients with IE, 213 (42%) of whom were PWID. Sixteen percent of patients died within 90 days of admission, including 14% of PWID and 17% of non-PWID (P = .50). In a multivariable Cox proportional hazard model, injection drug use was associated with a higher mortality within the first 14 days of admission (adjusted hazard ratio [aHR], 2.33 [95% confidence interval {CI}, 1.16-4.65], P = .02); however, there was no association between injection drug use and mortality between 15 and 90 days of admission (aHR, 0.63 [95% CI, .31-1.30], P = .21). Conclusions: Overall 90-day mortality did not differ between PWID and non-PWID with IE, although PWID experienced a higher risk of death within 14 days of admission. These findings suggest that early IE diagnosis and treatment among PWID is critical to improving outcomes.

A Multidisciplinary Pathway for the Diagnosis and Treatment of Infectious Endocarditis.

Clinical pathways can be useful when disparate clinical-pathologic groups converge on a common diagnostic and therapeutic trajectory. The progressive increase in the incidence of endocarditis in the US has included higher-risk subjects whose candidacy for aggressive cardiac surgical intervention may be highly resource-intensive, prohibitively high risk, or delayed and possibly deferred by comorbidities. We sought to define the sequence, application, and resolution of multidisciplinary endocarditis team decision-making in 4 distinct clinical groups.

Speckle Tracking Analysis of Left Ventricular Systolic Function Following Traumatic Brain Injury: A Pilot Prospective Observational Cohort Study.

BACKGROUND: Systolic dysfunction and reduction in left ventricular ejection fraction (LVEF) has been documented after traumatic brain injury (TBI). Speckle tracking is an emerging technology for myocardial strain assessment which has been utilized to identify subclinical myocardial dysfunction, and is most commonly reported as global longitudinal strain (GLS). We examined myocardial strain and regional strain patterns following moderate-severe TBI. MATERIALS AND METHODS: We conducted a prospective cohort study of moderate-severe TBI patients (Glasgow Coma Scale≤12) and age/sex-matched controls. Transthoracic echocardiography was performed within the first day and 1 week following TBI. Myocardial function was assessed using both GLS and LVEF, and impaired systolic function was defined as GLS >-16% or LVEF ≤50%. Regional strain patterns and individual strain trajectories were examined. RESULTS: Thirty subjects were included, 15 patients with TBI and 15 age/sex-matched controls. Among patients with adequate echocardiographic windows, systolic dysfunction was observed in 2 (17%) patients using LVEF and 5 (38%) patients using GLS within the first day after TBI. Mean GLS was impaired in patients with TBI compared with controls (-16.4±3.8% vs. -20.7±1.8%, P=0.001). Regional myocardial examination revealed impaired strain primarily in the basal and mid-ventricular segments. There was no improvement in GLS from day 1 to day 7 (P=0.81). CONCLUSIONS: Myocardial strain abnormalities are common and persist for at least 1 week following moderate-severe TBI. Speckle tracking may be useful for the early diagnosis and monitoring of systolic dysfunction following TBI.

Association of Early Myocardial Workload and Mortality Following Severe Traumatic Brain Injury.

OBJECTIVES: To examine the impact of early myocardial workload on in-hospital mortality following isolated severe traumatic brain injury. DESIGN: Retrospective cohort study. SETTING: Data from the National Trauma Databank, a multicenter trauma registry operated by the American College of Surgeons, from 2007 to 2014. PATIENTS: Adult patients with isolated severe traumatic brain injury (defined as admission Glasgow Coma Scale < 8 and head Abbreviated Injury Score ≥ 4). INTERVENTIONS: Admission rate-pressure product, categorized into five levels based on published low, normal, and submaximal human thresholds: less than 5,000; 5,000-9,999; 10,000-14,999; 15,000-19,999; and greater than 20,000. MEASUREMENTS AND MAIN RESULTS: Data from 26,412 patients were analyzed. Most patients had a normal rate-pressure product (43%), 35% had elevated rate-pressure product, and 22% had depressed rate-pressure product at hospital admission. Compared with the normal rate-pressure product group, in-hospital mortality was 22 percentage points higher in the lowest rate-pressure product group (cumulative mortality, 50.2%; 95% CI, 43.6-56.9%) and 11 percentage points higher in the highest rate-pressure product group (cumulative mortality, 39.2%; 95% CI, 37.4-40.9%). The lowest rate-pressure product group was associated with a 50% increased risk of mortality, compared with the normal rate-pressure product group (adjusted relative risk, 1.50; 95% CI, 1.31-1.76%; p < 0.0001), and the highest rate-pressure product group was associated with a 25% increased risk of mortality, compared with the normal rate-pressure product group (adjusted relative risk, 1.25; 95% CI, 1.18-1.92%; p < 0.0001). This relationship was blunted with increasing age. Among patients with normotension, those with depressed and elevated rate-pressure products experienced increased mortality. CONCLUSIONS: Adults with severe traumatic brain injury experience heterogeneous myocardial workload profiles that have a "U-shaped" relationship with mortality, even in the presence of a normal blood pressure. Our findings are novel and suggest that cardiac performance is important following severe traumatic brain injury.

Early Systolic Dysfunction Following Traumatic Brain Injury: A Cohort Study.

OBJECTIVE: Prior studies have suggested that traumatic brain injury may affect cardiac function. Our study aims were to determine the frequency, longitudinal course, and admission risk factors for systolic dysfunction in patients with moderate-severe traumatic brain injury. DESIGN: Prospective cohort study. SETTING: Level 1 trauma center. MEASUREMENTS: Transthoracic echocardiogram within 1 day and over the first week after moderate-severe traumatic brain injury; transthoracic echocardiogram within 1 day after mild traumatic brain injury (comparison group). MEASUREMENTS AND MAIN RESULTS: Systolic function was assessed by transthoracic echocardiogram, and systolic dysfunction was defined as fractional shortening less than 25%. Multivariable Poisson regression models examined admission risk factors for systolic dysfunction. Systolic function in 32 patients with isolated moderate-severe traumatic brain injury and 32 patients with isolated mild traumatic brain injury (comparison group) was assessed with transthoracic echocardiogram. Seven (22%) moderate-severe traumatic brain injury and 0 (0%) mild traumatic brain injury patients had systolic dysfunction within the first day after injury (p < 0.01). All patients with early systolic dysfunction recovered in 1 week. Younger age (relative risk, 0.87; 95% CI, 0.79-0.94; for 1 yr increase in age) and lower admission Glasgow Coma Scale score (relative risk, 0.34; 95% CI, 0.20-0.58; for one unit increase in Glasgow Coma Scale) were independently associated with the development of systolic dysfunction among moderate-severe traumatic brain injury patients. CONCLUSIONS: Early systolic dysfunction can occur in previously healthy patients with moderate-severe traumatic brain injury, and it is reversible over the first week of hospitalization. Younger age and lower admission Glasgow Coma Scale score are independently associated with the development of systolic dysfunction after moderate-severe traumatic brain injury.

Association of Early Hemodynamic Profile and the Development of Systolic Dysfunction Following Traumatic Brain Injury.

BACKGROUND: While systolic dysfunction has been observed following traumatic brain injury (TBI), the relationship between early hemodynamics and the development of systolic dysfunction has not been investigated. Our study aimed to determine the early hemodynamic profile that is associated with the development of systolic dysfunction after TBI. METHODS: We conducted a prospective cohort study among patients under 65 years old without cardiac comorbidities who sustained moderate-severe TBI. Transthoracic echocardiography was performed within the first day after TBI to assess for systolic dysfunction. Hourly systolic blood pressure (SBP), mean arterial pressure (MAP), heart rate, and confounding clinical variables (sedatives, fluid balance, vasopressors, and osmotherapy) were collected during the first 24 h following admission. Multivariable linear mixed models assessed the early hemodynamic profile in patients who developed systolic dysfunction, compared to patients who did not develop systolic dysfunction. RESULTS: Thirty-two patients were included, and 7 (22 %) developed systolic dysfunction after TBI. Patients who developed systolic dysfunction experienced early elevation of SBP, MAP, and heart rate, compared to patients who did not develop systolic dysfunction (p < 0.01 for all comparisons). Patients who developed systolic dysfunction experienced a greater rate of decrease in SBP [-10.2 mmHg (95 % CI -16.1, -4.2)] and MAP [-9.1 mmHg (95 % CI -13.9, -4.3)] over the first day of hospitalization, compared to patients who did not develop systolic dysfunction (p < 0.01 for both comparisons). All sensitivity analyses revealed no substantial changes from the primary model. CONCLUSIONS: Patients who develop systolic dysfunction following TBI have a distinctive hemodynamic profile, with early hypertension and tachycardia, followed by a decrease in blood pressure over the first day after TBI. This profile suggests an early maladaptive catecholamine-excess state as a potential underlying mechanism of TBI-induced systolic dysfunction.

Cardiac Dysfunction After Neurologic Injury: What Do We Know and Where Are We Going?

Recent literature has implicated severe neurologic injuries, such as aneurysmal subarachnoid hemorrhage, as a cause of cardiac dysfunction, impaired hemodynamic function, and poor outcomes. Mechanistic links between the brain and the heart have been explored in detail over the past several decades, and catecholamine excess, neuroendocrine dysfunction, and unchecked inflammation all likely contribute to the pathophysiologic process. Although cardiac dysfunction has also been described in other disease paradigms, including septic shock and thermal injury, there is likely a common underlying pathophysiology. In this review, we will examine the pathophysiology of cardiac dysfunction after neurologic injury, discuss the evidence surrounding cardiac dysfunction after different neurologic injuries, and suggest future research goals to gain knowledge and improve outcomes in this patient population.

Cardiac dysfunction following brain death in children: prevalence, normalization, and transplantation.

OBJECTIVES: Cardiac dysfunction has been reported to occur in as much as 42% of adults with brain death, and may limit cardiac donation after brain death. Knowledge of the prevalence and natural course of cardiac dysfunction after brain death may help to improve screening and transplant practices but adequately sized studies in pediatric brain death are lacking. The aims of our study are to describe the prevalence and course of cardiac dysfunction after pediatric brain death. DESIGN: Cross-sectional study. SETTING/SUBJECTS: We examined an organ procurement organization database (Life Center Northwest) of potential pediatric cardiac donors diagnosed with brain death between January 2011 and November 2013. INTERVENTION: Transthoracic echocardiograms were reviewed for cardiac dysfunction (defined as ejection fraction <50% or the presence of regional wall motion abnormalities). Descriptive statistics were used to analyze clinical characteristics and describe longitudinal echocardiogram findings in a subgroup of patients. We examined for heterogeneity between cardiac dysfunction with respect to cause of brain death. MEASUREMENT AND MAIN RESULTS: We identified 60 potential pediatric cardiac donors (age ≤ 18 yr) with at least one transthoracic echocardiogram following brain death. Cardiac dysfunction was present in 23 patients (38%) with brain death. Mean ejection fraction (37.6% vs 62.2%) and proportion of procured hearts (56.5% vs 83.8%) differed significantly between the groups with and without cardiac dysfunction, respectively. Of the 11 subjects with serial transthoracic echocardiogram data, the majority of patients with cardiac dysfunction (73%) improved over time, leading to organ procurement. No heterogeneity between cardiac dysfunction and particular causes of brain death was observed. CONCLUSION: The frequency of cardiac dysfunction in children with brain death is high. Serial transthoracic echocardiograms in patients with cardiac dysfunction showed improvement of cardiac function in most patients, suggesting that initial decisions to procure should not solely depend on the initial transthoracic echocardiogram examination results.

Temporal Changes in Left Ventricular Systolic Function and Use of Echocardiography in Adult Heart Donors.

BACKGROUND: One reason for refusal of donor hearts is the development of left ventricular systolic dysfunction, a condition reported to occur in up to 42 % of adults with brain death. Prior studies have suggested that appropriate donor management and evaluation of cardiac dysfunction with serial echocardiography (TTE) can improve organ procurement. The aims of our study are to examine the prevalence and describe longitudinal changes in cardiac dysfunction after brain death. METHODS: A cross-sectional study was performed using the Life Center Northwest organ database to identify potential adult heart donors diagnosed with brain death between January 2011 and November 2013. 246 potential donors with at least one TTE following brain death were identified. 58 donors received serial TTEs. Echocardiograms were reviewed for cardiac dysfunction, defined as left ventricular ejection fraction (EF) <50 % and/or presence of regional wall motion abnormalities. RESULTS: Cardiac dysfunction was present in 74 (30 %) patients. Age, body mass index, EF, and proportion of harvested organs differed significantly between the groups with and without cardiac dysfunction. Among patients receiving serial TTEs, 29 patients had cardiac dysfunction on initial TTE, with 15 (52 %) of these patients demonstrating resolved cardiac dysfunction over time leading to organ harvest. CONCLUSIONS: To our knowledge, the present study is the largest study describing the use of serial TTE and its utilization in adult donors. The prevalence of cardiac dysfunction after adult brain death is high, but given enough time and support, many of these donors have improvement in cardiac function, ultimately leading to transplantation.

Two pediatric cases of variant neurogenic stress cardiomyopathy after intracranial hemorrhage.

Takotsubo cardiomyopathy, also known as stress-induced cardiomyopathy, is an acquired form of left ventricular systolic dysfunction seen in the setting of physiologic stress and the absence of coronary artery disease. It is thought to be caused by excessive sympathetic stimulation. It is well described in the adult literature associated with subarachnoid hemorrhage where it is known as neurogenic stress cardiomyopathy (NSC), but few such pediatric cases have been reported. We describe our experience with 2 children (13- and 10-year-old girls) who presented with spontaneous intracranial hemorrhage followed by pulmonary edema and shock. Echocardiography revealed similar patterns of left ventricular wall motion abnormalities consistent with NSC, inverted Takotsubo variant. One child progressed to death, whereas the other made a remarkable recovery, including significant improvement in cardiac function over the course of 1 week. We argue that at least 1 of these cases represents true stress-induced cardiomyopathy. This report will alert pediatricians to this transient cardiomyopathy that is likely underdiagnosed in pediatric intensive care. We also highlight the challenges of managing both shock and elevated intracranial pressure in the setting of NSC.

Association between electrocardiographic findings and cardiac dysfunction in adult isolated traumatic brain injury.

INTRODUCTION: Abnormal electrocardiographic (ECG) findings can be seen in traumatic brain injury (TBI) patients. ECG may be an inexpensive tool to identify patients at high risk for developing cardiac dysfunction after TBI. The aim of this study was to examine abnormal ECG findings after isolated TBI and their association with true cardiac dysfunction, based on echocardiogram. METHODS: Data from adult patients with isolated TBI between 2003 and 2010 was retrospectively examined. Inclusion criteria included the presence of a 12-lead ECG within 24 h of admission and a formal echocardiographic examination within 72 h of admission after TBI. Patients with preexisting cardiac disease were excluded. Baseline clinical characteristics, 12-lead ECG, and echocardiogram report were abstracted. Logistic regression was used to identify the relationship of specific ECG abnormalities with cardiac dysfunction. RESULTS: We examined data from 59 patients with isolated TBI who underwent 12-lead ECG and echocardiographic evaluation. In this cohort, 13 (22%) patients had tachycardia (heart rate >100 bpm), 25 (42.4%) patients had a prolonged QTc, and 6 (10.2%) patients had morphologic end-repolarization abnormalities (MERA), with each having an association with abnormal echocardiographic findings: Odds ratios (and 95% confidence intervals) were 4.14 (1.02-17.05), 9.0 (1.74-46.65), and 5.63 (1.96-32.94), respectively. Ischemic-like ECG changes were not associated with echocardiographic abnormalities. CONCLUSIONS: Repolarization abnormalities (prolonged QTc and MERA), but not ischemic-like ECG changes, are associated with cardiac dysfunction after isolated TBI. 12-lead ECG may be an inexpensive screening tool to evaluate isolated TBI patients for cardiac dysfunction prior to more expensive or invasive studies.

The effect of feeding structured triacylglycerols enriched in eicosapentaenoic or docosahexaenoic acids on murine splenocyte fatty acid composition and leucocyte phagocytosis.

The effects of altering the type of n-3 polyunsaturated fatty acid (PUFA) in the mouse diet on the ability of monocytes and neutrophils to perform phagocytosis were investigated. Male weanling mice were fed for 7 d on one of nine diets which contained 178 g lipid/kg and which differed in the type of n-3 PUFA and in the position of these in dietary triacylglycerol (TAG). The control diet contained 4.4 g alpha-linolenic acid/100 g total fatty acids. In the other diets, eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) replaced a proportion (50 or 100 %) of the alpha-linolenic acid, and were in the sn-2 or the sn-1(3) position of dietary TAG. There were significant increases in the content of n-3 PUFA in spleen-cell phospholipids when EPA or DHA was fed. These increases were largely independent of the position of EPA or DHA in dietary TAG except when EPA was fed at the highest level, when the incorporation was greater when it was fed in the sn-2 than in the sn-1(3) position. There was no significant effect of dietary DHA on monocyte or neutrophil phagocytic activity. Dietary EPA dose-dependently decreased the number of monocytes and neutrophils performing phagocytosis. However, when EPA was fed in the sn-2 position, the ability of active monocytes or neutrophils to engulf bacteria was increased in a dose-dependent fashion. This did not occur when EPA was fed in the sn-1(3) position. Thus, there appears to be an influence of the position of EPA, but not of DHA, in dietary TAG on its incorporation into cell phospholipids and on the activity of phagocytic cells.

One-armed brachiation in gibbons (Hylobates lar).

The locomotor and postural behavior of Hylobates lar was studied in a seminaturalistic environment at the New York Zoological Park. A particular locomotor pattern, one-armed brachiation, was observed and filmed. Analysis indicated that the occurrence of one-armed brachiation as a preferred locomotor pattern was rare and was limited to the carrying of food. The limb and joint movements of one-armed brachiation closely resembled those of two-armed brachiation with differences occurring in the angular rotations of the support and the free arms. Analysis showed how a gibbon could maximize its forward momentum during one-armed brachiation. The adaptive value of one-armed brachiation is discussed in reference to brachiating while carrying food and to brachiating with a fracture of a forelimb. Finally, one-armed brachiation is discussed as an example of the concepts of locomotor totipotentiality and locomotor habit.