The global burden of atherosclerotic cardiovascular disease has risen from 271 million people in 1990 to more than 600 million people in 2023. Atherosclerotic vascular disease results not only from lipid accumulation within the arterial walls but also from acute and chronic inflammatory changes in response to arterial endothelial injury. Inflammation together with cytokines, chemokines, and acute-phase reactants play a pivotal role in atherosclerotic vascular plaque formation, progression, rupture, and thrombogenesis that lead to an acute coronary syndrome (ACS) or stroke. In addition, individuals who have previously sustained an ACS frequently have evidence of residual arterial inflammation as indicated by increased blood concentrations of the inflammatory biomarker C-reactive protein (CRP). As a consequence, chronic arterial inflammatory disease contributes to more than 15% of all global deaths from myocardial infarction, cerebral vascular events (transient ischemic attacks or strokes), and peripheral vascular disease. This Review Article discusses the important mechanisms by which inflammation contributes to the initiation and progression of coronary artery atherosclerosis, the biologic measurements which indicate arterial inflammation in individuals, the diagnostic techniques useful in the detection of arterial inflammation and atherosclerosis, and the clinical studies that have been performed and are currently being performed to limit the contributions of acute and chronic inflammation to the morbidity and mortality from coronary artery atherosclerosis.
Background: Infective endocarditis after transcatheter aortic valve implantation (TAVI-IE) is an uncommon but severe complication associated with substantial morbidity and mortality. Therapeutic strategies vary widely, since invasive management is often precluded by prohibitive risk and conservative medical therapy may be linked to poorer outcomes. Therefore, we aimed to compare outcomes between conservative and invasive management in patients with TAVI-IE.
Methods: A systematic search of PubMed, Scopus, and Web of Science identified comparative studies evaluating conservative versus invasive treatment in TAVI-IE. The primary endpoints were all-cause in-hospital and 1-year mortality. Pooled risk ratios (RRs) with 95% confidence intervals (CIs) were calculated using a random-effects model. Heterogeneity was quantified with I², publication bias was assessed with Egger's test, and sensitivity analyses (leave-one-out, GOSH plots) were performed.
Results: The search yielded 2,551 records; 15 studies met inclusion criteria for data extraction and meta-analysis. No significant differences were observed between conservative and invasive strategies for in-hospital mortality (RR 0.99, 95% CI 0.80-1.24, p=0.96; I²=0% with p=0.67) or 1-year mortality (RR 1.03, 95% CI 0.84-1.26; p=0.81; I²=11.4% with p=0.33). There was no evidence of publication bias (Egger's test: in-hospital, p=0.07; 1-year, p=0.54). Results were robust in sensitivity analyses.
Conclusions: In patients with TAVI-IE, conservative and invasive treatments were associated with comparable in-hospital and 1-year mortality. These findings support individualized, multidisciplinary decision-making rather than presuming a uniform advantage of either approach.

