Prioritizing public health? Factors affecting the issuance of stay-at-home orders in response to COVID-19 in Africa.

COVID-19 has sickened and killed millions of people globally. Conventional non-pharmaceutical interventions, particularly stay-at-home orders (SAHOs), though effective for limiting the spread of disease have significantly disrupted social and economic systems. The effects also have been dramatic in Africa, where many states are already vulnerable due to their developmental status. This study is designed to test hypotheses derived from the public health policymaking literature regarding the roles played by medical and political factors as well as social, economic, and external factors in African countries' issuance of SAHOs in response to the early stages of the COVID-19 pandemic. Using event history analysis, this study analyzed these five common factors related to public health policy to determine their impact on African states' varying decisions regarding the issuance of SAHOs. The results of this analysis suggest that medical factors significantly influenced decisions as did factors external to the states, while the role of political factors was limited. Social and economic factors played no discernible role. Overall, this study suggests how African leaders prioritized competing factors in the early stages of a public health crisis.

Human security as biosecurity Reconceptualizing national security threats in the time of COVID-19.

Research within security studies has struggled to determine whether infectious disease (ID) represents an existential threat to national and international security. With the emergence of SARS-CoV-2 (COVID-19), it is imperative to reexamine the relationship between ID and global security. This article addresses the specific threat to security from COVID-19, asking, "Is COVID-19 a threat to national and international security?" To investigate this question, this article uses two theoretical approaches: human security and biosecurity. It argues that COVID-19 is a threat to global security by the ontological crisis posed to individuals through human security theory and through high politics, as evidenced by biosecurity. By viewing security threats through the lens of the individual and the state, it becomes clear that ID should be considered an international security threat. This article examines the relevant literature and applies the theoretical framework to a case study analysis focused on the United States.

CHA2DS2-VASc and readmission with new-onset atrial fibrillation, atrial flutter, or acute cerebrovascular accident.

BACKGROUND: Although risk factors for atrial fibrillation (AF) and atrial flutter (AFL) are known, identifying patients who will develop AF/AFL within the near future remains challenging. We sought to evaluate if the CHA2DS2-VASc risk score (CVRS) can identify hospital readmissions with AF, AFL, or acute cerebrovascular accident (CVA) among hospitalized patients without prior history of AF/AFL. METHODS: Using the Nationwide Readmission Database, a study cohort included patients without prior AF/AFL or new diagnosis of AF/AFL at the index hospitalization from 2012 to 2014. Patients were stratified based on the CVRS into three groups: Low (CVRS ≤1), Intermediate (CVRS 2-5), and High (CVRS ≥6).The primary outcome of interest was 180-day readmission rate with a primary or secondary diagnosis of AF/AFL. Secondary outcomes of interest were acute CVA and 6-month mortality rate. RESULTS: A total of 17,820,640 patients were included in our study. Over a 6-month follow up duration from the index hospitalization, the overall re-admission rate for new onset atrial arrhythmias (AF/AFL) was 3.48% (n = 620,986), acute CVA 0.13% (n = 22,522), and all-cause mortality 0.31% (n = 55,632). When compared to other groups, patients with a higher CVRS were readmitted more frequently for AF/AFL [odds ratio (OR) 2.43; 95% confidence interval (CI) 2.41-2.45, P < .0001), acute CVA (OR 3.96; 95%CI 3.85-4.08, P < .0001), and all-cause mortality (OR 2.19; 95%CI 2.14-2.24, P < .0001). CONCLUSION: In this large contemporary cohort, a CHADS2VA2SC score ≥ 6 identified patients without known prior atrial arrhythmias at an elevated risk of developing AF/AFL or acute CVA within 6 months of hospitalization.

Delays in Presentation in Patients With Acute Myocardial Infarction During the COVID-19 Pandemic.

BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, has had a major impact on the behavior of patients, as well as on the delivery of healthcare services. With older and more medically vulnerable people tending to stay at home to avoid contracting the virus, it is unclear how the behavior of people with acute myocardial infarction (AMI) has changed. The aim of this study was to determine if delays in presentation and healthcare service delivery for AMI exist during the COVID-19 pandemic compared to the same period a year prior. METHODS: In this single-center, retrospective study, we evaluated patients admitted with ST-segment elevation myocardial infarction (STEMI) or non-ST-segment elevation myocardial infarction (NSTEMI) during early months of the COVID-19 pandemic (March 11, 2020 to April 20, 2020) compared to patients admitted with same diagnosis during the same period a year prior. RESULTS: There were 30 and 62 patients who presented with NSTEMI in the pandemic and pre-pandemic eras, respectively. The median pain-to-door time was significantly larger during the pandemic compared to pre-pandemic era (1,885 (880, 5,732) vs. 606 (388, 944) min, P < 0.0001). There was a significant delay in door-to-reperfusion time during the pandemic with a median time of 332 (182, 581) vs. 194 (92, 329) min (P = 0.0371). There were 24 (80%) and 25 (42%) patients who presented after 12 h of pain onset in pandemic and pre-pandemic eras, respectively (P = 0.0006). There were 47 and 60 patients who presented with STEMI during the pandemic timeframe of study and pre-pandemic timeframe, respectively. The median pain-to-door time during the pandemic was significantly larger than that of the pre-pandemic (620 (255, 1,500) vs. 349 (146, 659) min, P = 0.0141). There were 22 (47%) and 14 (24%) patients who presented after 12 h of pain onset in the pandemic and pre-pandemic eras, respectively (P = 0.0127). There was not a significant delay in door-to-reperfusion time (P = 0.9833). There were no differences in in-hospital death, stroke, or length of hospitalization between early and late presenters, as well as between pandemic and pre-pandemic eras. CONCLUSIONS: In conclusion, this study found that patients waited significantly longer during the pandemic to seek medical treatment for AMI compared to before the pandemic, and that pandemic-specific protocols may delay revascularization for NSTEMI patients. These findings resulted in more than a threefold increase from the onset of symptoms to revascularization increasing the risks for future complications such as left ventricular dysfunction and cardiovascular death. Efforts should be made to increase patients' awareness regarding consequences of delayed presentation, and to find a balance between hospital evaluation strategies and goals of minimizing total ischemic time.

Flecainide Toxicity Resulting in Pacemaker Latency and Intermittent Failure to Capture.

BACKGROUND Flecainide is a class Ic antiarrhythmic agent used in the treatment of supraventricular and ventricular arrhythmias. It is associated with a potent adverse effect profile; however, the effects of flecainide toxicity in the setting of a pacemaker have not been well described. We describe a unique case of flecainide toxicity secondary to acute kidney injury in the setting of a dual-chamber pacemaker, resulting in ventricular capture latency and intermittent failure to capture. CASE REPORT The patient was a 91-year-old female with a history of atrial fibrillation maintained in sinus rhythm on flecainide, who presented complaining of purple visual disturbances and syncope. She was found to be hypotensive and bradycardic, with a heart rate between 30 to 40 beats per minute. Lab work was notable for creatinine at 2.12 mg/dL. A 12-lead ECG demonstrated atrial and ventricular pacing with severely widened QRS complex and a significant latency between the pacemaker ventricular spike and the ventricular capture. The pacemaker was interrogated, revealing a significant increase in ventricular threshold from 0.75 V at 0.5 ms at baseline to 5.0 V at 1 ms to obtain consistent capture. After multiple boluses of IV sodium bicarbonate, the QRS acutely narrowed, latency interval improved, and consistent pacing capture was achieved. The flecainide level drawn on arrival was 3.09 mcg/mL. CONCLUSIONS Flecainide increases the ventricular capture threshold for pacemakers. Toxicity in these patients may present with pacemaker ventricular capture latency or failure to capture.

Use of AngioVac for Removal of Tricuspid Valve Vegetation.

The use is reported of the AngioVac system to resolve a case of persistent bacteremia in the setting of MRSA tricuspid valve infective endocarditis. The infection was secondary to intravenous drug use in a patient who had failed multiple antibiotic regimens and was deemed a poor surgical candidate.

Immunity, Inflammation, and Oxidative Stress in Heart Failure: Emerging Molecular Targets.

PURPOSE: Heart failure (HF) remains a major cause of morbidity and mortality worldwide. Although various therapies developed over the last two decades have shown improved long term outcomes in patients with established HF, there has been little progress in preventing the adverse cardiac remodeling that initiates HF. To fill the gap in treatment, current research efforts are focused on understanding novel mechanisms and signaling pathways. Immune activation, inflammation, oxidative stress, alterations in mitochondrial bioenergetics, and autophagy have been postulated as important pathophysiological events in this process. An improved understanding of these complex processes could facilitate a therapeutic shift toward molecular targets that can potentially alter the course of HF. METHODS: In this review, we address the role of immunity, inflammation, and oxidative stress as well as other novel emerging concepts in the pathophysiology of HF that may have therapeutic implications. CONCLUSION: Based on the experimental and clinical studies presented here, we anticipate that a better understanding of the pathophysiology of HF will open the door for new therapeutic targets. A one-size-fits-all approach may not be appropriate for all patients with HF, and further clinical trials utilizing molecular targeting in HF may result in improved outcomes.

The Effect of Metformin Use on Left Ventricular Ejection Fraction and Mortality Post-Myocardial Infarction.

BACKGROUND: Animal studies showed that the use of metformin after myocardial infarction (MI) resulted in a protective effect on cardiac myocytes. In this study, we examined the effect of metformin in patients with diabetes mellitus (DM) on left ventricular ejection fraction (LVEF) and post-MI mortality. METHODS: We reviewed charts of patients with MI admitted to the UAMS medical center. Baseline characteristics and 12-month follow up data were collected. Patients were classified into three groups: Control group- no DM (n = 464), Metformin group- DM + MI (n = 88) and No-Metformin group- DM + MI (n = 168). First, we compared Metformin and No-Metformin groups to the Control group. Second, we performed propensity-score matching in patients with DM, and compared Metformin to No-Metformin groups. RESULTS: All-cause 30-day and 12-month mortality was significantly higher in the No-Metformin group compared to controls (13.5 vs 9.3% p = 0.03 at 30 days, 23.7 vs 15.9 % p = 0.03 at 12 months). However, all-cause 30-day and 12-month mortality were similar in the Controls and Metformin group (9.3 vs 6.8 % p = 0.93 at 30 days, 15.9 vs 11.4 % p = 0.97 at 12 months). Mean LVEF on presentation (45 % in the three groups) and at follow up (47.84, 46.38 and 43.62 % in Control, Metformin, and No-Metformin groups, respectively) were not statistically different. There were no significant differences in regard to re-hospitalization, re-intervention, new stroke, CHF development, new MI, or identifiable arrhythmias. Metformin was an independent predictor of lower 30-day and 12-month all-cause mortality in patients with DM (HR 0.25, p = 0.02 and HR 0.32, p = 0.01, respectively). In the matched analysis, 30-day all-cause mortality was significantly higher in the No-Metformin compared to the Metformin group (21.1 vs 8.8 %, p = 0.05). However the difference in 12-month all-cause mortality did not reach statistical significance (24.6 vs 15.8 %, p = 0.15). CONCLUSION: This proof-of-concept study shows that use of metformin in patients with DM is associated with lower 30-day all-cause mortality and tendency for a lower 12-month all-cause mortality following MI without discernible improvement in LVEF.