Improving Confidence in ACLS among UMKC Internal Medicine Residents

"The American Board of Internal Medicine requires all residents to have their certification in basic life support (BLS) and advanced cardiovascular life support (ACLS) renewed every two years. However, there is concern that residents do not retain the confidence and the medical knowledge gained during this course throughout the two years that follow. The goal of our quality improvement project was to add a training workshop to improve resident confidence in performing ACLS."Ray Segebrecht, Anweshan Samanta, Laith Derbas, Alison Scharber, Ahmed Elkaryoni, Annapoorna Singh, Rahul Myadam, Adnan Choudhury, David Wooldridge, Ashraf Gohar, and Julie Banderas (Department of Internal Medicine, School of Medicine, University of Missouri-Kansas City)Includes bibliographical reference

Vitamin D3 Induces Mesenchymal-to-Endothelial Transition and Promotes a Proangiogenic Niche Through IGF-1 Signaling

Biological Sciences; Physiology; Molecular Biology; Cell Biolog

Separating Acute Rheumatic Fever from Nonrheumatic Streptococcal Myocarditis

Introduction. Streptococcal pharyngitis has been historically complicated with systemic involvement manifesting as acute rheumatic fever, which is a serious condition that can lead to permanent damage to heart valves. A recent association between streptococcal pharyngitis and nonrheumatic heart disease is emerging in literature. We present a case of nonrheumatic streptococcal myocarditis diagnosed using cardiac MRI. Case Presentation. A 25-year-old male, presented with complaints of sore throat, nonproductive cough, fever, pleuritic chest pain, and progressive dyspnea for four days. The patient had elevated troponins at presentation of 0.47 (ng/L) that peaked at 4.0 (ng/L). ECG showed sinus rhythm and ST elevations in leads V2, V3, V4, and V5. NT-Pro-BNP was 1740. Transthoracic echocardiogram (TTE) showed reduced ejection fraction (EF) of 37% and global hypokinesis. The rapid strep test was positive for group A streptococcus and C-reactive protein was elevated at 161. Cardiac MRI demonstrated an EF of 53% and edema in the anterior wall without delayed gadolinium enhancement. Cardiac catheterization showed normal coronaries. Discussion. According to modified Jones criteria, the patient did not meet the full major or minor criteria to be diagnosed with acute rheumatic fever. The course of the nonrheumatic myocarditis is favorable and includes a full recovery of cardiac function, no involvement of cardiac valves, or long-term use of antibiotics. Conclusion. It is crucial to make a separate distinction between acute rheumatic fever and nonrheumatic myocarditis because this will have huge implications on management and long-term use of antibiotics. Cardiac imaging modalities can aid in distinction between the two disease entities

Adult bone marrow cell therapy for ischemic heart disease : evidence and insights from randomized controlled trials

RATIONALE: Notwithstanding the uncertainties regarding the outcomes of BMC therapy for heart repair, further insights are critically needed to improve this promising approach. OBJECTIVE: To delineate the true impact of BMC therapy for cardiac repair and gain insights for future trials through systematic review and meta-analysis of data from eligible randomized controlled trials (RCTs). METHODS AND RESULTS: Database searches through August 2014 identified forty-eight eligible RCTs (enrolling 2602 patients). Weighted mean differences for changes in left ventricular (LV) ejection fraction (EF), infarct size, LV end-systolic volume (LVESV), and LV end-diastolic volume (LVEDV) were analyzed with random-effects meta-analysis. Compared with standard therapy, BMC transplantation improved LVEF (2.92%; 95% confidence interval [CI], 1.91 to 3.92; P<0.00001), reduced infarct size (−2.25%; 95% CI, −3.55 to −0.95; P=0.0007) and LVESV (−6.37 ml; 95% CI, −8.95 to −3.80; P<0.00001), and tended to reduce LVEDV (−2.26 ml; 95% CI, −4.59 to 0.07; P=0.06). Similar effects were noted when data were analyzed after excluding studies with discrepancies in outcomes reporting. The benefits also persisted when cardiac catheterization was performed in control patients as well. Although imaging modalities partly influenced the outcomes, LVEF improved in BMC-treated patients when assessed by MRI. Early (<48h) BMC injection after MI was more effective in reducing infarct size, while BMC injection between 3 and 10 days proved superior toward improving systolic function. A minimum of 50 million BMCs seemed to be necessary, with limited additional benefits seen with increasing cell numbers. BMC therapy was safe and improved clinical outcomes, including all-cause mortality, recurrent MI, ventricular arrhythmia, and cerebrovascular accident (CVA) during follow-up, albeit with differences between acute MI and chronic IHD subgroups. CONCLUSIONS: Transplantation of adult BMCs improves LVEF, reduces infarct size and ameliorates remodeling in patients with IHD. These effects are upheld in analyses of studies employing MRI, and also after excluding studies with discrepant outcomes reporting. BMC transplantation may also reduce the incidence of death, recurrent MI, ventricular arrhythmia, and CVA during follow-up

Adjunctive ablation strategies improve the efficacy of pulmonary vein isolation in non-paroxysmal atrial fibrillation: a systematic review and meta-analysis.

BACKGROUND: Pulmonary vein (PV) isolation (PVI) has suboptimal outcomes in patients with non-paroxysmal atrial fibrillation (AF). Adjunctive strategies employed to ablate non-PV triggers have shown favorable outcomes. AIMS: To delineate the incremental benefit of adjunctive ablation in patients with non-paroxysmal AF through a meta-analysis. METHODS AND RESULTS: Database searches through August 2016 identified five non-randomized and seven randomized controlled trials (enrolling 1694 patients). The adjunctive strategies employed for non-PV ablation included focal impulse and rotor modulation; empirical linear lines, ablation of complex fractionated atrial electrograms and ganglionated plexi. The risk ratio (RR) for AF recurrence, calculated with random effects meta-analysis showed a 36% reduction of AF recurrence at a median follow up of 12 months (RR: 0.64, 95% Confidence interval: 0.48 to 0.85; p = 0.003). The benefits persisted during longer follow up when assessed in subgroup analysis. CONCLUSIONS: Addition of adjunctive ablation to PVI improves outcomes

Correction: STAT3 balances myocyte hypertrophy vis-à-vis autophagy in response to Angiotensin II by modulating the AMPKα/mTOR axis.

[This corrects the article DOI: 10.1371/journal.pone.0179835.]

Transplantation of Human Umbilical Cord Blood–Derived Cellular Fraction Improves Left Ventricular Function and Remodeling After Myocardial Ischemia/Reperfusion

Rationale: Human umbilical cord blood (hUCB) contains diverse populations of stem/progenitor cells. Whether hUCB-derived nonhematopoietic cells would induce cardiac repair remains unknown. Objective: To examine whether intramyocardial transplantation of hUCB-derived CD45 Lin nonhematopoietic cellular fraction after a reperfused myocardial infarction in nonimmunosuppressed rats would improve cardiac function and ameliorate ventricular remodeling. Methods and Results: Nonhematopoietic CD45−Lin− cells were isolated from hUCB. Flow cytometry and quantitative polymerase chain reaction were used to characterize this subpopulation. Age-matched male Fischer 344 rats underwent a 30-minute coronary occlusion followed by reperfusion and 48 hours later received intramyocardial injection of vehicle or hUCB CD45−Lin− cells. After 35 days, compared with vehicle-treated rats, CD45−Lin− cell–treated rats exhibited improved left ventricular function, blunted left ventricular hypertrophy, greater preservation of viable myocardium in the infarct zone, and superior left ventricular remodeling. Mechanistically, hUCB CD45−Lin− cell injection favorably modulated molecular pathways regulating myocardial fibrosis, cardiomyocyte apoptosis, angiogenesis, and inflammation in postinfarct ventricular myocardium. Rare persistent transplanted human cells could be detected at both 4 and 35 days after myocardial infarction. Conclusion: Transplantation of hUCB-derived CD45−Lin− nonhematopoietic cellular subfraction after a reperfused myocardial infarction in nonimmunosuppressed rats ameliorates left ventricular dysfunction and improves remodeling via favorable paracrine modulation of molecular pathways. These findings with human cells in a clinically relevant model of myocardial ischemia/reperfusion in immunocompetent animals may have significant translational implications.Visual Overview: An online visual overview is available for this article

STAT3 balances myocyte hypertrophy vis-à-vis autophagy in response to Angiotensin II by modulating the AMPKα/mTOR axis

<div><p>Signal transducers and activators of transcription 3 (STAT3) is known to participate in various cardiovascular signal transduction pathways, including those responsible for cardiac hypertrophy and cytoprotection. However, the role of STAT3 signaling in cardiomyocyte autophagy remains unclear. We tested the hypothesis that Angiotensin II (Ang II)-induced cardiomyocyte hypertrophy is effected, at least in part, through STAT3-mediated inhibition of cellular autophagy. In H9c2 cells, Ang II treatment resulted in STAT3 activation and cellular hypertrophy in a dose-dependent manner. Ang II enhanced autophagy, albeit without impacting AMPKα/mTOR signaling or cellular ADP/ATP ratio. Pharmacologic inhibition of STAT3 with WP1066 suppressed Ang II-induced myocyte hypertrophy and mRNA expression of hypertrophy-related genes ANP and β-MHC. These molecular events were recapitulated in cells with STAT3 knockdown. Genetic or pharmacologic inhibition of STAT3 significantly increased myocyte ADP/ATP ratio and enhanced autophagy through AMPKα/mTOR signaling. Pharmacologic activation and inhibition of AMPKα attenuated and exaggerated, respectively, the effects of Ang II on ANP and β-MHC gene expression, while concomitant inhibition of STAT3 accentuated the inhibition of hypertrophy. Together, these data indicate that novel nongenomic effects of STAT3 influence myocyte energy status and modulate AMPKα/mTOR signaling and autophagy to balance the transcriptional hypertrophic response to Ang II stimulation. These findings may have significant relevance for various cardiovascular pathological processes mediated by Ang II signaling.</p></div