What Causes Premature Coronary Artery Disease?

PURPOSE OF REVIEW: This review provides an overview of genetic and non-genetic causes of premature coronary artery disease (pCAD). RECENT FINDINGS: pCAD refers to coronary artery disease (CAD) occurring before the age of 65 years in women and 55 years in men. Both genetic and non-genetic risk factors may contribute to the onset of pCAD. Recent advances in the genetic epidemiology of pCAD have revealed the importance of both monogenic and polygenic contributions to pCAD. Familial hypercholesterolemia (FH) is the most common monogenic disorder associated with atherosclerotic pCAD. However, clinical overreliance on monogenic genes can result in overlooked genetic causes of pCAD, especially polygenic contributions. Non-genetic factors, notably smoking and drug use, are also important contributors to pCAD. Cigarette smoking has been observed in 25.5% of pCAD patients relative to 12.2% of non-pCAD patients. Finally, myocardial infarction (MI) associated with spontaneous coronary artery dissection (SCAD) may result in similar clinical presentations as atherosclerotic pCAD. Recognizing the genetic and non-genetic causes underlying pCAD is important for appropriate prevention and treatment. Despite recent progress, pCAD remains incompletely understood, highlighting the need for both awareness and research.

Dexmedetomidine as adjunct treatment for severe alcohol withdrawal in the ICU.

BACKGROUND: Patients undergoing alcohol withdrawal in the intensive care unit (ICU) often require escalating doses of benzodiazepines and not uncommonly require intubation and mechanical ventilation for airway protection. This may lead to complications and prolonged ICU stays. Experimental studies and single case reports suggest the α2-agonist dexmedetomidine is effective in managing the autonomic symptoms seen with alcohol withdrawal. We report a retrospective analysis of 20 ICU patients treated with dexmedetomidine for benzodiazepine-refractory alcohol withdrawal. METHODS: Records from a 23-bed mixed medical-surgical ICU were abstracted from November 2008 to November 2010 for patients who received dexmedetomidine for alcohol withdrawal. The main analysis compared alcohol withdrawal severity scores and medication doses for 24 h before dexmedetomidine therapy with values during the first 24 h of dexmedetomidine therapy. RESULTS: There was a 61.5% reduction in benzodiazepine dosing after initiation of dexmedetomidine (n = 17; p < 0.001) and a 21.1% reduction in alcohol withdrawal severity score (n = 11; p = .015). Patients experienced less tachycardia and systolic hypertension following dexmedetomidine initiation. One patient out of 20 required intubation. A serious adverse effect occurred in one patient, in whom dexmedetomidine was discontinued for two 9-second asystolic pauses noted on telemetry. CONCLUSIONS: This observational study suggests that dexmedetomidine therapy for severe alcohol withdrawal is associated with substantially reduced benzodiazepine dosing, a decrease in alcohol withdrawal scoring and blunted hyperadrenergic cardiovascular response to ethanol abstinence. In this series, there was a low rate of mechanical ventilation associated with the above strategy. One of 20 patients suffered two 9-second asystolic pauses, which did not recur after dexmedetomidine discontinuation. Prospective trials are warranted to compare adjunct treatment with dexmedetomidine versus standard benzodiazepine therapy.

Fluoroquinolone utilization in the emergency departments of academic medical centers: prevalence of, and risk factors for, inappropriate use.

BACKGROUND: Resistance to fluoroquinolone (FQ) antibiotics has risen markedly in recent years and has been associated with increasing FQ use; however, few data exist regarding FQ use patterns. Designing strategies to limit FQ resistance by optimizing FQ use depends on identifying patterns of inappropriate FQ use. Use of FQs in emergency departments (EDs) has not been studied. METHODS: We studied 100 consecutive ED patients who received an FQ and were subsequently discharged. Appropriateness of the indication for use was judged according to existing institutional guidelines. A case-control study was conducted to identify the prevalence of, and risk factors for, inappropriate FQ use. RESULTS: Of 100 total patients, 81 received an FQ for an inappropriate indication. Of these cases, 43 (53%) were judged inappropriate because another agent was considered first line, 27 (33%) because there was no evidence of infection based on the documented evaluation, and 11 (14%) because of inability to assess the need for antimicrobial therapy. Although the prevalence of inappropriate use was similar across various clinical scenarios, there was a borderline significant association between the hospital in which the ED was located and inappropriate FQ use. Of the 19 patients who received an FQ for an appropriate indication, only 1 received both the correct dose and duration of therapy. CONCLUSIONS: Inappropriate FQ use in EDs is extremely common. Efforts to limit emergence of FQ resistance must address the high level of inappropriate FQ use in EDs. Future studies should evaluate the impact of interventions designed to reduce inappropriate FQ use in this setting.