Atherothrombosis and high-risk plaque: part I: evolving concepts

Atherothrombosis is a complex disease in which cholesterol deposition, inflammation, and thrombus formation play a major role. Rupture of high-risk, vulnerable plaques is responsible for coronary thrombosis, the main cause of unstable angina, acute myocardial infarction, and sudden cardiac death. In addition to rupture, plaque erosion may also lead to occlusive thrombosis and acute coronary events. Atherothrombosis can be evaluated according to histologic criteria, most commonly categorized by the American Heart Association (AHA) classification. However, this classification does not include the thin cap fibroatheroma, the most common form of high-risk, vulnerable plaque. Furthermore, the AHA classification does not include plaque erosion. As a result, new classifications have emerged and are reviewed in this article. The disease is asymptomatic during a long period and dramatically changes its course when complicated by thrombosis. This is summarized in five phases, from early lesions to plaque rupture, followed by plaque healing and fibrocalcification. For the early phases, the role of endothelial dysfunction, cholesterol transport, high-density lipoprotein, and proteoglycans are discussed. Furthermore, the innate and adaptive immune response to autoantigens, the Toll-like receptors, and the mechanisms of calcification are carefully analyzed. For the advanced phases, the role of eccentric remodeling, vasa vasorum neovascularization, and mechanisms of plaque rupture are systematically evaluated. In the final thrombosis section, focal and circulating tissue factor associated with apoptotic macrophages and circulatory monocytes is examined, closing the link between inflammation, plaque rupture, and blood thrombogenicity.     

Sudden cardiac death: mechanisms, therapies and challenges

Sudden cardiac death (SCD) is the leading cause of cardiac death in the US. In the past few years, intensive efforts have been made to expand public awareness of SCD and to increase our understanding of its pathophysiology, medical treatment options and device therapy. Significant advances have been made in our ability to prevent SCD in both primary and secondary health care. Two critical issues remain, however: the identification of patients who would benefit from such therapies, and how to achieve even greater prevention, especially primary prevention. The goal of this article is to provide a review of the topic of SCD in the setting of abnormal myocardial substrate, to outline the techniques that are useful in identifying patients at risk, and available treatment options.     

International Impact of COVID-19 on the Diagnosis of Heart Disease

BackgroundThe coronavirus disease 2019 (COVID-19) pandemic has adversely affected diagnosis and treatment of noncommunicable diseases. Its effects on delivery of diagnostic care for cardiovascular disease, which remains the leading cause of death worldwide, have not been quantified.ObjectivesThe study sought to assess COVID-19’s impact on global cardiovascular diagnostic procedural volumes and safety practices.MethodsThe International Atomic Energy Agency conducted a worldwide survey assessing alterations in cardiovascular procedure volumes and safety practices resulting from COVID-19. Noninvasive and invasive cardiac testing volumes were obtained from participating sites for March and April 2020 and compared with those from March 2019. Availability of personal protective equipment and pandemic-related testing practice changes were ascertained.ResultsSurveys were submitted from 909 inpatient and outpatient centers performing cardiac diagnostic procedures, in 108 countries. Procedure volumes decreased 42% from March 2019 to March 2020, and 64% from March 2019 to April 2020. Transthoracic echocardiography decreased by 59%, transesophageal echocardiography 76%, and stress tests 78%, which varied between stress modalities. Coronary angiography (invasive or computed tomography) decreased 55% (p < 0.001 for each procedure). In multivariable regression, significantly greater reduction in procedures occurred for centers in countries with lower gross domestic product. Location in a low-income and lower–middle-income country was associated with an additional 22% reduction in cardiac procedures and less availability of personal protective equipment and telehealth.ConclusionsCOVID-19 was associated with a significant and abrupt reduction in cardiovascular diagnostic testing across the globe, especially affecting the world’s economically challenged. Further study of cardiovascular outcomes and COVID-19–related changes in care delivery is warranted.     

Impact of HIV-1 replication on immunological evolution during long-term dual-boosted protease inhibitor therapy

To explore CD4-cell and viral evolution in relation to different levels of HIV-1 replication, as observed during protease inhibitor (PI)-based antiretroviral therapy. Adult HIV-1 infected cohort patients, receiving historical salvage therapy with daily doses of saquinavir (2,000 mg), ritonavir (200 mg) and either lopinavir (800 mg) or atazanavir (300 mg) for >36 weeks were retrospectively analysed for highest detectable viral load up to week 96 and assigned to groups according to the viral load level: always <50 copies/ml (1), 50–199 copies/ml (2), 200–499 copies/ml (3) and ≥500 copies/ml (4). A total of 126 patients were evaluated; at baseline, median CD4-cell count was 204/mm³, HIV-1 RNA was 5.13 Log10-copies/ml and duration of prior HIV-1 infection was 11.7 years. Patients were assigned by 43, 30, 7 and 20 % to groups 1–4. Median observation time was 136 weeks (range: 38–304); at weeks 48/96, the CD4-cell gains for groups 1–4 were +88/+209, +209/+349, +67/+300 and +114.5/+ 128, respectively. After fitting data in a linear fixed effect model, ascending CD4 slopes were continuously increasing for group 1, similarly for 2 and clearly decreasing for 3–4 (p = 0.0006). Of 25 individuals from group 4, patient number with major IAS-USA protease mutations increased from 5 to 10 before and after failing PI therapy, whereas minor mutations remained stable (n = 18). On double-boosted PI therapy, CD4-cell increases through week 96 were similar for patients at always undetectable or with detection of low viral load. Viral detection >200 copies/ml was associated with decreasing CD4-cell slopes and emergence of major mutations, supporting this as benchmark for virological failure definition on PI therapy.     

Mapping the microbiological diversity of odontogenic abscess: are we using the right drugs?

Objectives

The aim of this study was categorizing the microbial flora and susceptibility to antibiotics and to clarify to which degree the empiric administered antibiotics are suitable for therapy.

Materials and methods

A 3.5-year retrospective study evaluated hospital records of 206 patients who suffered from head and neck infections of odontogenic origin. All patients underwent surgical incision and drainage and received intravenous antibiotics and inpatient treatment. The specimens were obtained by performing a swab.

Results

Two hundred six patients were included with 251 strains isolated (1.22 per patient). One hundred eight strains showed antibiotic resistance. Eighty-seven patients showed at least one bacterial strain that showed antibiotic resistance (42.2%). The most frequent isolated bacteria were Streptococcus spp. (n = 116), with a high rate of antibiotic resistance (50.8%). We investigated 205 cases of antibiotic resistance in 87 subjects. Nine bacterial strains showed no susceptibility to unacid (4.3%) and 36 strains to clindamycin (17.5%).

Conclusion

Antibiotic resistance against clindamycin was rather high. The distribution of the afflicted spaces and isolated bacteria was alike recent findings. It is mandatory to understand that immediate surgical treatment in terms of incision and drainage is the basis in abscess treatment. Antibiotic treatment is adjunct therapy.

Clinical relevance

Streptococcus species were the most frequently identified bacteria presenting antibiotic resistance in more than 50%. Increased resistant rates for clindamycin require reconsiderations regarding an empiric antibiotic treatment.

     

Peri-implant bone preservation of a novel,self-cutting,and fully tapered implant in the healed crestal ridge of minipigs: submerged vs. transgingival healing

Clinical Oral Investigations - The aim of this study was to assess the influence of transgingival compared with submerged healing on peri-implant bone maintenance around a novel, fully tapered...     

Impact of environmental factors in predicting daily severity scores of atopic dermatitis

BackgroundAtopic dermatitis (AD) is a chronic inflammatory skin disease that affects 20% of children worldwide. Environmental factors including weather and air pollutants have been shown to be associated with AD symptoms. However, the time‐dependent nature of such a relationship has not been adequately investigated. This paper aims to assess whether real‐time data on weather and air pollutants can make short‐term prediction of AD severity scores.MethodsUsing longitudinal data from a published panel study of 177 paediatric patients followed up daily for 17 months, we developed a statistical machine learning model to predict daily AD severity scores for individual study participants. Exposures consisted of daily meteorological variables and concentrations of air pollutants, and outcomes were daily recordings of scores for six AD signs. We developed a mixed‐effect autoregressive ordinal logistic regression model, validated it in a forward‐chaining setting and evaluated the effects of the environmental factors on the predictive performance.ResultsOur model successfully made daily prediction of the AD severity scores, and the predictive performance was not improved by the addition of measured environmental factors. Potential short‐term influence of environmental exposures on daily AD severity scores was outweighed by the underlying persistence of preceding scores.ConclusionsOur data does not offer enough evidence to support a claim that weather or air pollutants can make short‐term prediction of AD signs. Inferences about the magnitude of the effect of environmental factors on AD severity scores require consideration of their time‐dependent dynamic nature.