Impact of Deliberate Practice on Point-of-Care Ultrasound Interpretation of Right Ventricle Pathology.

Background: Point-of-care (POC) ultrasound (POCUS) has become an essential tool in caring for critically ill patients in several specialties. Mastery in POCUS requires competency in image acquisition, image interpretation, and integration into clinical care. Deliberate practice is an effective method for performance improvement in many areas of medical education; however, it is not well described in the literature for POCUS training. Objective: To analyze differences in the effect of deliberate practice in POCUS image interpretation on performance improvement in groups with varying skill levels. Methods: We recruited attending physicians and trainees with varying degrees of expertise in POCUS to complete a 50-item educational instrument on the interpretation of right ventricle size and function. The instrument incorporated deliberate practice for the task of correctly identifying right ventricle size and function as either normal or abnormal. Pulmonary critical care trainees obtained and interpreted POCUS images of patients with diagnosed acute pulmonary embolism, which were compared with gold-standard, two-dimensional echocardiographic scans obtained by an expert technician and interpreted by a cardiologist board-certified in echocardiography. We mapped learners' cumulative accuracy on a learning curve to assess their performance. In addition, we compared groups on the basis of prior experience with using POC echocardiography. Results: Seventy-nine of 81 participants completed the survey and examination and were included in the analysis. Of the participants, 69 (87.3%) were trainees. The overall cumulative accuracy for the group was 72.9%. All groups demonstrated improvement in accuracy with repetitive practice. Conclusion: Deliberate practice in POC echocardiograph interpretation is effective for improving performance in a wide range of learners. Further study is needed to define accuracy cutoffs for competency to help guide learning plans and program requirements and for application into a model for global POC echocardiography competence.

Reducing length of stay with the direct oral anti-coagulants in low and intermediate risk pulmonary embolism: a single center experience.

Direct oral anti-coagulants (DOACs) reduce hospital length-of-stay (LOS) in patients with acute pulmonary embolism (PE) in clinical trials. There is a paucity of literature describing real world utility of DOACs, particularly in intermediate-risk patients. To evaluate if the utilization of DOACs vs. non-DOACs in acute PE patients, reduces LOS without a difference in safety in patients defined as low and intermediate-risk of mortality by the European Society of Cardiology. This was a retrospective cohort study of prospectively collected data from a single center registry of consecutive adult outpatients diagnosed with acute PE who survived to hospital discharge. Primary outcome was median hospital LOS. Secondary outcomes were 30-day readmission, survival, and incidence of major and minor bleeding. There were 307 outpatients admitted with acute PE 88 (28.7%) low-risk, 213 (69.4%) intermediate-risk, and 6 (2.0%) high-risk. Two hundred and twenty-six (73.6%) received a DOAC. There was a statistically significant shorter median LOS in all patients treated with a DOAC (2.9 days, IQR 1.8-4.7) vs non-DOAC (4.9 days, IQR 3-8.9) (Generalized Linear Model p < 0.001). There was a shorter median LOS between intermediate-risk patients treated with a DOAC (3.6 days, IQR 2-5.8) vs non-DOAC (5, IQR 3-9). There was no difference in 30-day readmission, survival, or bleeding complications in both cohorts. There was a reduction in LOS in low and intermediate risk patients treated with a DOAC without a difference in 30-day safety and efficacy. Treating acute PE patients with DOACs including intermediate-risk patients, compared to conventional anticoagulation, may facilitate early discharge, and potentially reduce hospital costs.

A narrative review of red blood cell distribution width as a marker for pulmonary embolism.

Red blood cell distribution width (RDW) is a marker of variability in red blood cell size, and is routinely reported as part of a patient's complete blood count. RDW has been shown to be associated with the prediction, severity and prognosis of pulmonary embolism (PE) in recent studies. The underlying biomolecular mechanism of the relationship of RDW to PE is largely unknown, but is thought to be due to the relationship of RDW with acute inflammatory markers and variations in blood viscosity. This review substantiates that a high RDW level, defined using either an arbitrary number or according to receiver operator curve statistics, is associated with a higher risk of acute PE, increased severity (massive vs. submassive) of PE and increased mortality in patients with PE. Nevertheless, the comparison of current studies is limited due to the definition of high RDW (each study uses a different RDW cutoff level), the broad range of exclusion criteria and the inclusion of differing modalities used to diagnose a PE (computed tomography angiogram, ventilation-perfusion study, or clinical diagnosis). Despite the above limitations, these studies provide a promising future clinical use for RDW as a marker of PE.

Right Heart Thrombi: Patient Outcomes by Treatment Modality and Predictors of Mortality: A Pooled Analysis.

RATIONALE: Right heart thrombi (RiHT) is characterized by the presence of thrombus within the right atrium or right ventricle (RV). Current literature suggests pulmonary embolism (PE) with RiHT carries a high mortality. Guidelines lack recommendations in managing RiHT. We created a pooled analysis on RiHT and report on our institutional experience in managing RiHT. We aimed to evaluate whether patient characteristics and differing treatment modalities predict mortality. METHODS: We created a pooled analysis of case reports and series of patients with RiHT and PE between January 1956 and 2017. We also reviewed a series of consecutive patients with RiHT identified from our institutional PE registry. Age, shock, RV dysfunction, clot mobility, treatment modality, and hospital outcome had to be reported. RESULTS: We identified 316 patients in our pooled analysis. Patients received the following therapies: no treatment 15 (5%), systemic anticoagulation 73 (23%), systemic thrombolysis 108 (34%), surgical embolectomy 101 (32%), catheter-directed therapy 11 (3%), and systemic thrombolysis with surgery 8 (3%). In-hospital mortality was 18.7%. Univariate analysis showed age and shock reduced odds of survival. Multivariate analysis showed shock reduced odds of survival (odds ratios [OR] 0.36, 95% confidence interval [CI]: 0.19-0.72, P ≤ .01) while age, RV dysfunction, and clot-mobility did not affect mortality. In a reduced multivariate analysis adjusting for shock, treatment modality, and clot location alone, systemic thrombolysis increased odds of survival when compared to systemic anticoagulation (OR 2.72, 95% CI: 1.11-6.64, P = .02). Our institutional series identified 18 patients, where in-hospital mortality was 22.2%, 18 (100%) had RV dysfunction, and 5 (28%) had shock. Patients received the following therapies: systemic anticoagulation 8 (44.4%), systemic thrombolysis 4 (22.2%), surgical embolectomy 4 (22.2%), and catheter-directed thrombolysis 2 (11.1%). CONCLUSION: Presence of shock in RiHT is an independent predictor of mortality. Systemic thrombolysis may offer increased odds of survival when compared to systemic anticoagulation. Our findings should be interpreted with caution as they derive from retrospective reports and subject to publication bias.

Pulmonary infarction secondary to pulmonary embolism: An evolving paradigm.

BACKGROUND AND OBJECTIVE: Pulmonary infarction (PI) from pulmonary embolism (PE) remains an entity of unclear aetiology. PI has been thought to occur in elderly patients with cardiopulmonary disease. We hypothesize younger patients without cardiopulmonary comorbidities are at highest risk. Our study aims to characterize PI clinically and radiographically, determine associated risk factors and determine their clinical significance. METHODS: We conducted a single-centre retrospective review of 367 consecutive patients with PE. Clinical and radiographic data were compared between patients with and without PI using chi-square and F-tests. Univariate and multivariate analyses were performed to evaluate risk factors for PI. RESULTS: PI occurred in 62 of 367 patients with acute PE (16.9%). Patients with PI were significantly younger (48 ± 20.3 vs 59.6 ± 17.2 years, P < 0.01), with lower pulmonary embolism severity index (PESI) scores (73.7 ± 38.1 vs 91.9 ± 37.5 years, P < 0.01) and endorsed chest pain with significantly higher frequency (65% vs 39%, P < 0.01). There was no significant difference in other clinical symptoms, hospital length of stay or mortality between groups. Presence of radiographic cardiopulmonary disease was significantly lower in patients with PI (emphysema: 5% vs 22%, P = <0.01; aortic atherosclerosis: 23% vs 43%, P = <0.01). In multivariate analysis, age ≤33 (OR 3.5 CI: 1.37-8.95, P < 0.01), chest pain (OR 2.15 CI: 1.15-4.00, P = 0.02) and pleural effusion (OR 2.18 CI: 1.08-4.41, P = 0.03) increased PI risk and presence of emphysema decreased risk (OR 0.21 CI: 0.06-0.70, P = 0.01). CONCLUSION: Younger patients without cardiopulmonary comorbidities are at highest risk of PI. Chest pain and pleural effusion significantly increased risk of PI while presence of radiographic emphysema reduced risk.

Diagnostic Accuracy of Point-of-Care Ultrasound Performed by Pulmonary Critical Care Physicians for Right Ventricle Assessment in Patients With Acute Pulmonary Embolism.

OBJECTIVES: Risk stratification for acute pulmonary embolism using imaging presence of right ventricular dysfunction is essential for triage; however, comprehensive transthoracic echocardiography has limited availability. We assessed the accuracy and timeliness of Pulmonary Critical Care Medicine Fellow's performance of goal-directed echocardiograms and intensivists' interpretations for evaluating right ventricular dysfunction in acute pulmonary embolism. DESIGN: Prospective observational study and retrospective chart review. SETTING: Four hundred fifty bed urban teaching hospital. PATIENTS: Adult in/outpatients diagnosed with acute pulmonary embolism. INTERVENTIONS: Pulmonary critical care fellows performed and documented their goal-directed echocardiogram as normal or abnormal for right ventricular size and function in patients with acute pulmonary embolism. Gold standard transthoracic echocardiography was performed on schedule unless the goal-directed echocardiogram showed critical findings. Attending intensivists blinded to the clinical scenario reviewed these exams at a later date. MEASUREMENTS AND MAIN RESULTS: Two hundred eighty-seven consecutive patients were evaluated for acute PE. Pulmonary Critical Care Medicine Fellows performed 154 goal-directed echocardiograms, 110 with complete cardiology-reviewed transthoracic echocardiography within 48 hours for comparison. Pulmonary Critical Care Medicine Fellow's area under the curve for size and function was 0.83 (95% CI, 0.75-0.90) and 0.83 (95% CI, 0.75-0.90), respectively. Intensivists' 1/2 area under the curve for size and function was (1) 0.87 (95% CI, 0.82-0.94), (1) 0.87 (95% CI, 0.80-0.93) and (2) 0.88 (95% CI, 0.82-0.95), (2) 0.88 (95% CI, 0.82-0.95). Median time difference between goal-directed echocardiogram and transthoracic echocardiography was 21 hours 18 minutes. CONCLUSIONS: This is the first study to evaluate pulmonary critical care fellows' and intensivists' use of goal-directed echocardiography in diagnosing right ventricular dysfunction in acute pulmonary embolism. Pulmonary Critical Care Medicine Fellows and intensivists made a timely and accurate assessment. Screening for right ventricular dysfunction using goal-directed echocardiography can and should be performed by pulmonary critical care physicians in patients with acute pulmonary embolism.

Impact of pocket ultrasound use by internal medicine housestaff in the diagnosis of dyspnea.

BACKGROUND: Recent reports demonstrate high diagnostic accuracy of lung ultrasound for evaluation of dyspnea. We assessed the feasibility of training internal medicine residents in lung ultrasound with a pocket ultrasound device. METHODS: We performed a prospective, observational trial of residents performing lung ultrasound with a pocket ultrasound. Training consisted of two 90-minute sessions of didactics and supervised bedside performance. Two residents received an additional 2 weeks of training. Residents recorded a clinical diagnosis based on admission data. Following lung ultrasound performance, an ultrasound diagnosis was recorded integrating clinical and sonographic findings. Using receiver operating curve analysis, the area under the curve was calculated for both clinical diagnosis and ultrasound diagnosis using attending physician's final discharge diagnosis as the gold standard. RESULTS: Five residents performed 69 exams. The AUC for ultrasound diagnosis was significantly higher than that for clinical diagnosis (0.87 vs 0.81, P < 0.01). AUCs increased using lung ultrasound for diagnoses as follows: chronic obstructive pulmonary disease (0.73-0.85, P = 0.06), acute pulmonary edema (0.85-0.89, P = 0.49), pneumonia (0.77-0.88, P = 0.01), and pleural effusions (0.76-0.96, P < 0.002). CONCLUSIONS: Lung ultrasound performed by residents with a pocket ultrasound improved the diagnostic accuracy of dyspnea. Two residents undergoing extended training showed a total increase in diagnostic accuracy.

Radiation-induced heart disease.

Radiation-induced heart disease (RIHD) is becoming an increasing concern for patients and clinicians alike as the use of radiation therapy for the treatment of certain malignancies increases, and patient mortality secondary to neoplasms of the thorax, in particular Hodgkin's lymphoma and breast cancer, decreases. The spectrum of pathology affecting the heart spans from acute to chronic and can affect almost all facets of the heart, including but not restricted to the pericardial sac, coronary arteries, myocardium, and heart valves. Significant research has been conducted over the past 40 years to further understand the toxic effects of radiation therapy and those protective methods that could curtail these adverse reactions. This article will focus on RIHD, the pathophysiological mechanisms for RIHD, the clinical presentations, and current and future directions for attempting to reduce the incidence of this condition.

Protein complexes at the microtubule organizing center regulate bipolar spindle assembly.

Bipolar spindle assembly is essential to genomic stability in dividing cells. Centrosomes or spindle pole bodies duplicated earlier at G(1)/S remain adjacent until triggered at mitotic onset to become bipolar. Pole reorientation is stabilized by microtubule interdigitation but mechanistic details for bipolarity remain incomplete. To investigate the contribution of spindle pole microtubule organizing center (MTOC) proteins in bipolarity, we applied genetic, structural and molecular biochemical analysis along with timelapse microscopy. Spindle formation was followed by an in vivo growth assay with the conditional allele cut7-22(ts), encoding fission yeast mitotic Kinesin-5, essential for bipolarity. By analysis of double and triple mutant strains of MTOC alleles and cut7-22(ts) we found that stabilized microtubules or increased bundling can rescue cut7-22(ts) associated bipolarity defects. These changes to microtubule dynamics and organization occurred through two surface domains on gamma-tubulin, a helix 11 domain and an adjacent site for binding MTOC protein Alp4. We demonstrate that Kinesin-14 Pkl1, known to oppose bipolarity, can bind to gamma-tubulin at helix 11 and that mutation of either of two conserved residues in helix 11 can impair Kinesin-14 binding. Altering the Alp4/gamma-tubulin interaction, conserved residues in helix 11 or deletion of pkl1 each are sufficient to rescue bipolarity in our cut7-22(ts) strain. Our findings provide novel insights into regulation of the bipolar mechanism through the MTOC complex.

Impact of iodinated contrast injections on percent diameter coronary arterial stenosis and implications for trials of intracoronary pharmacotherapies in patients with ST-elevation myocardial infarction.

Administration of fibrinolytic, antiplatelet, and antithrombotic agents by the intracoronary route may disaggregate clot, but the potential role of the mechanical force of the injection itself in decreasing clot burden has not been studied. Patients with ST-segment elevation myocardial infarction who were pretreated in the emergency room (ER) with unfractionated heparin and aspirin in the TITAN-TIMI 34 study were randomized to treatment with eptifibatide in the ER (n = 131) versus after diagnostic catheterization (n = 150). Quantitative coronary angiography was used to assess change in diameter stenosis from time of first contrast injection to injection before percutaneous coronary intervention (PCI) immediately preceding wire placement down the culprit artery in a matching view. Successful perfusion of the myocardium was assessed after PCI by the presence of Thrombolysis In Myocardial Infarction myocardial perfusion grade of 2 or 3. In patients treated with eptifibatide in the ER, there was a 1.3% absolute improvement in diameter stenosis from the first injection to the injection before PCI (p = 0.02), whereas there was no change in diameter stenosis in patients not treated with eptifibatide in the ER (0.0%, p = NS). Each 1% improvement in percent diameter stenosis during diagnostic injections before PCI was strongly correlated with an open muscle after PCI (adjusted odds ratio 1.09, 95% confidence interval 1.02 to 1.16, p = 0.012). In conclusion, the mechanical force of a contrast injection decreases thrombotic burden in patients with ST-segment elevation myocardial infarction pretreated with eptifibatide but not with placebo. Future trials of intracoronary pharmacotherapies should include a control arm in which saline is injected to account for the potential clot disaggregation that occurs as a result of iodinated contrast injections, particularly if the patient has been pretreated with aggressive pharmacotherapy.

Diagnostic and prognostic value of ambulatory ECG (Holter) monitoring in patients with coronary heart disease: a review.

Silent ischemia, the most common expression of atherosclerotic heart disease, affects approximately 30-50% of patients during their activities of daily living. The present review provides a comprehensive and practical summary of current knowledge on perioperative myocardial ischemia through MEDLINE searches up to June 2005, using keywords including "silent ischemia," "transient ischemia," and "Holter monitoring." Holter monitoring (i.e., continuous ambulatory ST-segment monitoring) is an effective tool for assessing the frequency and duration of silent transient myocardial ischemia, particularly in patients who are post-acute myocardial infarction (MI), those with acute coronary syndromes (ACS), and in patients in the acute post-operative period. Holter monitoring allows for further risk stratification of patients who have a positive exercise ECG by collecting long-term ECG data on ischemic and arrhythmic events while patients perform routine activities. Both the presence and increased duration of transient ischemia as detected by continuous ST-segment Holter monitoring are associated with increased rates of coronary events and mortality. Holter monitoring may aid in the identification of patients and subgroups of patients with ACS who may derive the greatest benefit from antiplatelet and antithrombotic therapy. Indeed, many ongoing and upcoming trials of pharmacotherapy include ischemia on Holter monitoring as an endpoint.

An extended anaphase signaling pathway for Mad2p includes microtubule organizing center proteins and multiple motor-dependent transitions.

Signaling pathways within the mitotic mechanism temporally orchestrate spindle assembly with chromosome capture and alignment, and then coordinate initiation of chromosome segregation with spindle breakdown and cytokinesis for reproductive success. Kinetochore localized Mad2p acts in the spindle assembly checkpoint pathway during prophase and prometaphase to monitor bipolar attachment of chromosomes to spindle microtubules as well as proper tension at kinetochores. Once established, Mad2p is not degraded, but instead transits to spindle poles preceding the metaphase/anaphase transition in human and yeast cells. Whether conserved relocalization of Mad2p to poles is a final step in the spindle assembly checkpoint pathway or whether the post-metaphase transition allows Mad2p to cooperate in anaphase events leading to mitotic exit has been unknown. We examined post-metaphase localization of Mad2p in fission yeast. Our observations indicate an extended signaling pathway for Mad2p that includes kinetochore to bipolar localization at spindle poles, then additional transitions from bipolar to unipolar to equatorial. We determined that Mad2p associates with the microtubule organizing center complex through direct binding to Alp4p and that microtubule motor proteins Kinesin-14 Pkl1 and Dynein contribute to Mad2p anaphase transitions. At anaphase B onset, bipolar to unipolar transitions of both Mad2p and the septation inititiation network (SIN) kinase Cdc7 are observed. We determined that Mad2p and Cdc7p transitions monitor different events in anaphase, but that neither are required for anaphase B initiation. Our findings indicate that altered Mad2p anaphase spindle localizations can reflect changes in spindle function during mitotic exit that could contribute to fidelity in anaphase events.