Coronavirus disease 2019 and cardiovascular diseases: collateral damage?

PURPOSE OF REVIEW: Cardiovascular involvement in coronavirus disease 2019 (COVID-19) is relatively common and portends an increased risk of morbidity and mortality. Manifestations of myocardial injury may exhibit significant overlap and result in diagnostic uncertainty. This review will summarize recent literature around cardiovascular complications of COVID-19. RECENT FINDINGS: Venous thromboembolism, atrial fibrillation, and type II myocardial infarction are observed commonly in COVID-19, while severe acute respiratory syndrome coronavirus 2 viral myocarditis remains quite rare. Although infrequent, COVID-19 vaccination has been associated with myocarditis and pericarditis in young individuals. SUMMARY: Various forms of COVID-19-related myocardial injury have been associated with increased utilization of mechanical ventilation, hemodynamic deterioration, and mortality. Manifestations of myocardial injury in COVID-19 are varied, but share common drivers of illness including sequelae of sepsis, immune-mediated factors, and a prothrombotic state. Understanding the forms of myocardial injury in COVID-19 may aid in rapid diagnosis and treatment.

Successful Intravascular Lithotripsy Use for Acute Stent Underexpansion in Saphenous Vein Grafts.

Experience with intravascular lithotripsy (IVL) following stent deployment in saphenous vein graft (SVG) lesions is limited. We present 2 cases of percutaneous intervention in SVG in which acute stent underexpansion was successfully managed with IVL. In the first case, recalcitrant plaque required prestent deployment IVL, with intracoronary imaging showing persistent calcification. Additional poststent deployment IVL facilitated full expansion and successful stent delivery. In the second case, predilation with semicompliant balloons appeared angiographically effective, but stent deployment showed acute underexpansion. Postdilation with noncompliant balloons and ultimately IVL allowed full expansion and successful stent delivery. These are the first reported cases of IVL use immediately after stent deployment in SVG to treat underexpansion due to recalcitrant calcification.

Dislodged Coronary Stents: The Presnaring Technique.

When dislodged stents remain on the coronary wire, the wire can be snared outside of the body (presnaring), and the snare loop advanced over the wire into the body to retrieve the stent. Presnaring may be a valuable technique to retrieve dislodged coronary stents when the stent remains on the coronary wire, as demonstrated in the 2 patients described.

Patterns of Care and Outcomes of Ambulatory Endovascular Interventions in Lower Extremity Peripheral Arterial Disease.

Lower extremity endovascular intervention (LE-EVI) is gaining popularity as the primary treatment modality for patients with symptomatic peripheral artery disease refractory to noninvasive management. We examined the contemporary patterns of care, regional variation, and outcomes of ambulatory LE-EVI in the United States. The National Ambulatory Surgery Sample was analyzed to identify 266,563 records with peripheral artery disease and LE-EVI between January 1, 2016 and December 31, 2017. The mean age of the study cohort was 68.9 years and 40.5% were women. The majority of the endovascular interventions were performed at large (58.1%), urban teaching (64.1%), private not-for-profit (76.8%) centers, and the southern region accounted for most cases (43%). Periprocedural major adverse renal and cardiovascular events and other complications were 0.5% and 3.3%, respectively. Most patients (97.6%) were discharged home after the procedure. Age, female gender, uncontrolled hypertension, ischemic heart disease, heart failure, arrhythmia, chronic kidney disease, malnutrition, non-Medicare insurance, private for-profit, urban teaching facilities, and southern and midwest regions were associated with higher odds of major adverse renal and cardiovascular events. The mean charges per patient encounter were $56,500, with significant differences across various patient and facility characteristics. In conclusion, our study demonstrates the use, patterns of care, financial aspect, and overall safety of ambulatory LE-EVIs in a real-world setting.

Scenes from the past: multidetector CT of Egyptian mummies of the Redpath Museum.

As a nondestructive method of historical and anthropologic inquiry, imaging has played an important role in mummy studies over the past several decades. Recent technologic advances have made multidetector computed tomography (CT) an especially useful means for deepening the present understanding of ancient cultures by examining preserved human remains. In April 2011, three ancient Egyptian human mummies from the Redpath Museum of McGill University were examined with 320-section multidetector CT as part of the IMPACT Radiological Mummy Database project headquartered at the University of Western Ontario. Whole-body scanning was performed with a section thickness of 0.5 mm and a peak voltage of 120 kVp, and the raw CT datasets were postprocessed by using smooth body and high-resolution bone convolution filters. Two of the mummies were scanned at different energy levels (80 and 135 keV). The high-resolution CT scans revealed the details of mummification and allowed observations about the socioeconomic and health status of the human subjects based on both the mummification technique used and the appearance of the remains, particularly the bones and teeth. The paleopathologic information obtained from the scans confirmed some findings in studies performed in the same mummies in the late 19th and 20th centuries. The CT scans also demonstrated a high degree of variability in Egyptian mortuary practice, variability that is not generally recognized in the literature. Unusual features that were observed included a relatively uncommon retained heart in mummy RM2718, retained lungs in a mummy from which the heart had been extracted (RM2720), and a cartonnage plaque placed over the left abdomen of a mummy that had been eviscerated transperineally (RM2717).

Nitric oxide mediates relative airway hyporesponsiveness to lipopolysaccharide in surfactant protein A-deficient mice.

Surfactant protein A (SP-A) mediates innate immune cell responses to LPS, a cell wall component of gram-negative bacteria that is found ubiquitously in the environment and is associated with adverse health effects. Inhaled LPS induces lung inflammation and increases airway responsiveness (AR). However, the role of SP-A in mediating LPS-induced AR is not well-defined. Nitric oxide (NO) is described as a potent bronchodilator, and previous studies showed that SP-A modulates the LPS-induced production of NO. Hence, we tested the hypothesis that increased AR, observed in response to aerosolized LPS exposure, would be significantly reduced in an SP-A-deficient condition. Wild-type (WT) and SP-A null (SP-A(-/-)) mice were challenged with aerosolized LPS. Results indicate that despite similar inflammatory indices, LPS-treated SP-A(-/-) mice had attenuated AR after methacholine challenge, compared with WT mice. The attenuated AR could not be attributed to inherent differences in SP-D concentrations or airway smooth muscle contractile and relaxation properties, because these measures were similar between WT and SP-A(-/-) mice. LPS-treated SP-A(-/-) mice, however, had elevated nitrite concentrations, inducible nitric oxide synthase (iNOS) expression, and NOS activity in their lungs. Moreover, the administration of the iNOS-specific inhibitor 1400W completely abrogated the attenuated AR. Thus, when exposed to aerosolized LPS, SP-A(-/-) mice demonstrate a relative airway hyporesponsiveness that appears to be mediated at least partly via an iNOS-dependent mechanism. These findings may have clinical significance, because recent studies reported associations between surfactant protein polymorphisms and a variety of lung diseases.

Learning and leadership in advanced dementia care.

This article, part of a series in Nursing Older People exploring the nursing care of people living with advanced dementia, considers learning and leadership. It outlines learning opportunities about advanced dementia and what developments are needed. The need for strong leadership at all levels and settings is explored along with the challenges of educating those who care for the person with advanced dementia. It also outlines educational opportunities and programmes before illustrating how one nurse leads advanced dementia care in practice.

Both hematopoietic-derived and non-hematopoietic-derived {beta}-arrestin-2 regulates murine allergic airway disease.

Allergic asthma, a major cause of morbidity and leading cause of hospitalizations, is an inflammatory disease orchestrated by T helper cells and characterized by the lung migration of eosinophils, which are important asthma effector cells. Lung migration of inflammatory cells requires, among other events, the chemokine receptor transduction of lung-produced inflammatory chemokines. Despite the widespread prevalence of this disease, the molecular mechanisms regulating chemokine production and receptor regulation in asthma are poorly understood. Previous work from our laboratory demonstrated that beta-arrestin-2 positively regulates the development of allergic airway disease in a mouse model, partly through positive regulation of T-lymphocyte chemotaxis to the lung. However, beta-arrestin-2 is expressed in many cell types, including other hematopoietic cells and lung structural cells, which are involved in the development and manifestation of allergic airway disease. To determine the cell types required for beta-arrestin-2-dependent allergic inflammation, we generated bone marrow chimera mice. Using the ovalbumin murine model of allergic airway disease, we show that eosinophilic and lymphocytic inflammation is restored in chimeric mice, with expression of beta-arrestin-2 exclusively on hematopoietic-derived cell types. In contrast, airway hyperresponsiveness is dependent on the expression of beta-arrestin-2 in structural cells. Our data demonstrate that the expression of beta-arrestin-2 in at least two divergent cell types contributes to the pathogenesis of allergic airway disease.

Erratum to: Efficacy of Coronary Computed Tomography Angiography for the De Novo Detection of Chronic Total Occlusion Prior to Coronary Angiography: A Preliminary and Retrospective Study.

[This corrects the article DOI: 10.1055/s-0040-1716328.].

Safety of Calcium-Channel Blockers During Radial Cardiac Catheterization in Patients With Acute Myocardial Infarction or Systolic Heart Failure.

OBJECTIVES: The aim of this study was to evaluate the safety of calcium-channel blockers (CCBs) during radial artery catheterization in two populations with a contraindication to their use. BACKGROUND: Cardiac catheterization performed via the radial approach has become increasingly common worldwide, but adoption has been slow in the United States. One possible explanation is concern over radial artery vasospasm, which can complicate procedures. Spasmolytic drugs, typically intra-arterial CCBs, are used to prevent spasm, but their safety is not well established in high-risk populations, such as those with ST-segment elevation myocardial infarction (STEMI) or systolic heart failure (HF), in which CCB may be contraindicated. METHODS: Consecutive STEMI and HF patients undergoing cardiac catheterization over a 1-year period were prospectively evaluated. All operators in our laboratory use the radial approach unless contraindicated. All patients received CCB immediately after sheath insertion. The primary outcome of interest was change in blood pressure immediately after CCB. Procedural outcomes were also evaluated. RESULTS: A total of 184 patients were included in the study (54 with STEMI and 129 with HF). There was a significant drop in systolic blood pressure (SBP) and diastolic blood pressure (DBP) following verapamil administration (P<.001 for both), but no change in HR (P>.99). SBP decreased more than 20 mm Hg in 15.7% of patients, none of whom required initiation of vasopressors. In regression analysis, only baseline SBP correlated significantly with the change in blood pressure. CONCLUSIONS: Patients with STEMI or HF can safely tolerate intra-arterial CCB during radial catheterization.

Beta-arrestin-2 regulates the development of allergic asthma.

Asthma is a chronic inflammatory disorder of the airways that is coordinated by Th2 cells in both human asthmatics and animal models of allergic asthma. Migration of Th2 cells to the lung is key to their inflammatory function and is regulated in large part by chemokine receptors, members of the seven-membrane-spanning receptor family. It has been reported recently that T cells lacking beta-arrestin-2, a G protein-coupled receptor regulatory protein, demonstrate impaired migration in vitro. Here we show that allergen-sensitized mice having a targeted deletion of the beta-arrestin-2 gene do not accumulate T lymphocytes in their airways, nor do they demonstrate other physiological and inflammatory features characteristic of asthma. In contrast, the airway inflammatory response to LPS, an event not coordinated by Th2 cells, is fully functional in mice lacking beta-arrestin-2. beta-arrestin-2-deficient mice demonstrate OVA-specific IgE responses, but have defective macrophage-derived chemokine-mediated CD4+ T cell migration to the lung. This report provides the first evidence that beta-arrestin-2 is required for the manifestation of allergic asthma. Because beta-arrestin-2 regulates the development of allergic inflammation at a proximal step in the inflammatory cascade, novel therapies focused on this protein may prove useful in the treatment of asthma.

Early dental intervention in the Redpath Ptolemaic Theban Male.

A computed tomography study of the remains of a Ptolemaic male mummy from Thebes (RM2718; 350-60 BCE), one of three ancient Egyptian human mummies curated at McGill University's Redpath Museum, demonstrates the packing of a large interproximal carious lesion with a protective linen barrier. The dental packing described here is unique among ancient Egyptian mummies studied to date, and represents one of only a few recorded dental interventions in ancient Egypt. Such a finding lends further support for the existence of a group of dental specialists practicing interventional medicine in ancient Egypt. While the physical evidence, to date for other interventions, may be scarce, the findings presented here should underline the need to continue to look for evidence of dental packing as well as other therapeutic dental interventions in the ancient world.

Toll-like receptor 4 antagonist (E5564) prevents the chronic airway response to inhaled lipopolysaccharide.

Although chronic inhalation of endotoxin or lipopolysaccharide (LPS) causes all of the classic features of asthma, including airway hyperreactivity, airway inflammation, and airway remodeling, the mechanisms involved in this process are not clearly understood. The objective of this study was to determine whether intratracheal treatment with LPS antagonist (E5564, a lipid A analog) prevented the development of chronic endotoxin-induced airway disease in a mouse model of environmental airway disease. Pretreatment with 10 and 100 microg of E5564 was found to inhibit the airway response (hyperreactivity and inflammation) for up to 48 h after the administration of the compound. Repeated dosing with 50 microg of E5564 intratracheally did not cause any measurable toxicity. Therefore, in a chronic experiment, mice were treated with either E5564 (50 microg) or vehicle three times weekly for 5 wk and simultaneously daily exposed to either LPS (4.65 +/- 0.30 microg/m3) or saline aerosol. E5564 was effective in decreasing the airway hyperreactivity to methacholine, the air space neutrophilia, the interleukin-6 in the lung lavage fluid, and the neutrophil infiltration of the airways 36 h after 5 wk of LPS inhalation. Less collagen deposition was observed in the airways of E5564-treated mice compared with vehicle-treated mice after a 4-wk recovery period. Our results indicate that E5564, a Toll-like receptor 4 antagonist, minimizes the physiological and biological effects of chronic LPS inhalation, suggesting a therapeutic role for competitive LPS antagonists in preventing or reducing endotoxin-induced environmental airway disease.