minocycline and Aortitis

Evidence from preclinical and clinical studies has demonstrated that myocardial infarction promotes atherosclerosis progression. The impact of focal vascular inflammation on the progression and phenotype of remote atherosclerosis remains unknown. Approach and Results: We used a novel. We show for the first time that focal arterial inflammation in response to vascular injury enhances systemic vascular inflammation, accelerates remote atheroma progression and induces plaques more inflamed, lipid-rich, and collagen-poor in the absence of ischemic myocardial injury. This inflammatory cascade is modulated by pravastatin and minocycline treatments, which have anti-inflammatory effects at both plaque and systemic levels that mitigate atheroma progression.

Topics: Animals; Anti-Inflammatory Agents; Aortitis; Atherosclerosis; Brachiocephalic Trunk; Collagen; Disease Models, Animal; Disease Progression; Inflammation Mediators; Interleukin-6; Lipid Metabolism; Male; Mice, Knockout, ApoE; Minocycline; Necrosis; Plaque, Atherosclerotic; Pravastatin; Time Factors

Non-typhoid Salmonella species represent a significant cause of aortitis. Few antimicrobial agents can be used when the patient is allergic or intolerable to cephalosporins or fluoroquinolones. Here, we report a case of bacteremia and aortitis caused by Salmonella enterica serotype Choleraesuis. This patient was cured by initial parenteral tigecycline and subsequent oral ciprofloxacin without surgical intervention.

Topics: Aged; Anti-Bacterial Agents; Aortitis; Bacteremia; Ciprofloxacin; Humans; Male; Minocycline; Salmonella arizonae; Salmonella enterica; Salmonella Infections; Tigecycline; Treatment Outcome