Clinical Medicine Insights. Cardiology最新文献

Background: Internal carotid artery stenosis is primarily attributed to atherosclerosis in the carotid artery bifurcation. Previous studies have detected oral bacteria in atherosclerotic lesions, suggesting an association between oral bacteria and atherosclerosis. In this study, we compared the bacterial flora of the atherosclerotic plaque in the carotid artery and dental plaque of patients with internal carotid artery stenosis using 16S ribosomal RNA (16S rRNA) metagenomic sequencing.

Methods: Fifty-four patients who underwent internal carotid endarterectomy for internal carotid artery stenosis at the Showa University Hospital between April 2016 and February 2018 were included. Polymerase chain reaction targeting the 16S rRNA gene detected bacterial DNA in the carotid plaques of 11 cases, of which only 5 could be further analyzed. Thereafter, DNA extracted from the carotid and oral plaques of these 5 cases were analyzed using metagenomic sequencing targeting 16S rRNA. In addition, their general condition and oral conditions were evaluated. The patients were classified into symptomatic and asymptomatic groups based on the presence or absence of symptoms of transient ischemic attack, and their bacterial flora was evaluated.

Results: The results demonstrated that the microflora of carotid plaques (n = 5) contained bacterial species from 55 families and 78 genera. In addition, 86.5% of the bacteria detected in the carotid plaques were also detected in oral plaques. Cariogenic and periodontopathic bacteria accounted for 27.7% and 4.7% of the bacteria in the carotid plaques, respectively.

Conclusions: These results suggest that oral bacteria are directly or indirectly involved in the pathogenesis of atherosclerosis. More extensive studies of oral commensal bacteria detected in extra-oral lesions are warranted to comprehensively investigate the role of oral bacteria in the pathogenesis of systemic diseases.

Introduction: A few months after the beginning of the coronavirus disease of 2019 (COVID-19) vaccination, several reports of myocarditis secondary to the vaccines were published, sometimes with fulminant cases, but until today there is no proven causal link between these 2 events, but with many hypotheses proposed.

Methods: A systematic review of current evidence regarding myocarditis after COVID-19 vaccination was performed by searching several databases including PubMed/Medline and Web of Science. The quality of Meta-analysis was assessed using the AMSTAR-2 tool as well as other qualitative criteria.

Results: Our umbrella review appraised 4 Meta-analysis of retrospective studies (range: 5-12), The number of vaccine doses included ranged from 12 to 179 million, with the number of myocarditis cases observed ranging from 343 to 1489. All types of vaccines were evaluated, with no exclusions. The overall incidence ranged from 0.89 to 2.36 cases of myocarditis per 100 000 doses of vaccine received. Heterogeny was assessed in 3 of the Meta-analysis, and was highly significant (>75%) in all included studies, and with a significant P-value (P < .05). Regarding publication bias, 3 of the Meta-analysis conducted the egger and begg regression, with a significant result in only 1. Regarding the assessment of the methodology by the AMSTAR-2 scale indicating that the quality was very critical in 1, low in 2, and moderate in 1 Meta-analysis.

Conclusion: The quality of current non-randomized evidence on real causality and incidence of myocarditis after COVID-19 vaccine is still low.

Preventing hypertension by restricting dietary salt intake, sodium chloride, is well established in public health policy, but a pathophysiological mechanism has yet to explain the controversial clinical finding that some individuals have a greater risk of hypertension from exposure to salt intake, termed salt-sensitive hypertension. The present perspective paper synthesizes interdisciplinary findings from the research literature and offers novel insights proposing that the pathogenesis of salt-sensitive hypertension is mediated by interaction of salt-induced hypervolemia and phosphate-induced vascular calcification. Arterial stiffness and blood pressure increase as calcification in the vascular media layer reduces arterial elasticity, preventing arteries from expanding to accommodate extracellular fluid overload in hypervolemia related to salt intake. Furthermore, phosphate has been found to be a direct inducer of vascular calcification. Reduction of dietary phosphate may help reduce salt-sensitive hypertension by lowering the prevalence and progression of vascular calcification. Further research should investigate the correlation of vascular calcification with salt-sensitive hypertension, and public health recommendations to prevent hypertension should encourage reductions of both sodium-induced hypervolemia and phosphate-induced vascular calcification.

Biventricular thrombi are a rare clinical entity and only reported in several case reports. Given ventricular thrombi are high risk for cardioembolic events, accurate detection and therapeutic management has an important influence on clinical outcomes. We present a case of a patient with biventricular thrombi that was initially diagnosed on computed tomography angiography, emphasizing its clinical utility as a rapid, non-invasive imaging modality for early detection.