Impact of Chronic Statin Therapy on Postprocedural Contrast-Induced Nephropathy in Patients Undergoing Non-Emergent Percutaneous Coronary Intervention.

BACKGROUND: Following percutaneous coronary intervention (PCI), elevations in serum creatinine level and declines in glomerular filtration rate are common. Prior studies have demonstrated benefit of chronic statin therapy in the prevention of contrast-induced nephropathy (CIN); however, it is unknown whether chronic statin therapy reduces the incidence of CIN in the non-emergent PCI setting. METHODS: Using the 2004-2005 Cornell Angioplasty Registry, a total of 1171 consecutive patients were selected for analysis. The population was divided into two groups: (1) patients on chronic (≥30 days) statin therapy prior to PCI (n = 874); and (2) patients not on chronic statin therapy (n = 297). RESULTS: Patients taking chronic statin therapy were more likely to have diabetes mellitus (35.7% vs 22.6%; P<.001), previous myocardial infarction (36.3% vs 20.5%; P<.001), previous PCI (38.9% vs 16.2%; P<.001), and previous coronary artery bypass graft surgery (19.5% vs 11.4%; P=.01). Statin users were also more likely to be taking long-term aspirin (77.8% vs 59.6%; P<.001) and clopidogrel therapy (29.9% vs 14.1%; P<.001). Baseline serum creatinine levels were comparable between the two groups, as were procedural characteristics. The incidence of CIN following PCI was not significantly different between patients on chronic statin therapy versus those not on chronic statin therapy (4.2% vs 5.4%; P=.42). However, after multivariate adjustment, chronic statin therapy was associated with a lower incidence of CIN (odds ratio [OR], 0.21; 95% confidence interval [CI], 0.05-0.94; P=.04). Acute heart failure on admission and the urgency of the procedure (urgent vs elective PCI) were also independent predictors for developing CIN (OR, 3.04; 95% CI, 1.45-6.66 [P=.01] and OR, 2.80; 95% CI, 1.42-5.55 [P=.01], respectively). Long-term mortality rates were similar between those on chronic statin therapy and those not on statins. CONCLUSION: CIN occurred in 4.5% of patients following non-emergent PCI. Multivariate analysis demonstrated that chronic statin therapy decreased the odds of developing CIN in patients undergoing PCI.

Analysis of intersegmental trough and proximal latency of smooth muscle contraction using high-resolution esophageal manometry.

BACKGROUND AND AIMS: Intersegmental troughs (ISTs) between striated and smooth muscle contraction segments on high-resolution manometry (HRM) have been linked to hypomotility disorders. We investigated the relationship between ISTs, latency of initiation of smooth muscle contraction, and motor patterns in symptomatic patients and normal controls. METHODS: HRM Clouse plots were analyzed in 199 participants (47.2±1.2 y, 112F/87M), categorized into 110 participants with gastroesophageal reflux disease (GERD), 74 symptomatic participants without GERD, and 15 healthy controls. IST length was measured in centimeters and percentage esophageal length, designated extended when ≥20% esophageal length on >30% swallows. Proximal latency was measured as the time interval between onset of skeletal and smooth muscle contraction segments, and designated prolonged when ≥4s in ≥50% of swallows. RESULTS: ISTs of any length were noted in 74.6% swallows and in 92.5% of participants, with a similar frequency across the 3 groups. ISTs and proximal latency were both longer in the GERD group, especially when Barrett esophagus was present, compared with non-GERD patients or controls (P≤0.03 across groups); extended IST and prolonged proximal latency followed similar trends. On multivariate logistic regression, extended IST predicted GERD [odds ratio (OR), 2.30; 95% confidence intervals (CI) 1.18-4.47], as did lower esophageal sphincter pressure <5 mm Hg (OR, 3.79-3.96; 95% CI 1.77-8.49), after controlling for age and sex; prolonged proximal latency predicted both GERD (OR, 2.03; 95% CI 1.01-4.12) and Barrett esophagus (OR 1.91, 95% CI 1.24-2.94). CONCLUSIONS: Measurement of IST and proximal latency add value to HRM analysis, and may be markers of esophageal hypomotility.

Methicillin-resistant Staphylococcus aureus USA300 clone as a cause of Lemierre's syndrome.

We describe a case of a young woman who had methicillin-resistant Staphylococcus aureus USA300 clone (MRSA-USA300)-associated Lemierre's syndrome and secondary necrotizing pneumonia and cerebral infarcts. We also review 11 cases of S. aureus-associated Lemierre's syndrome reported in the literature from 1965 to 2010. Recognition of S. aureus as an emergent cause of Lemierre's syndrome informs the initial empirical antibiotic choice for this life-threatening condition and may positively impact patient outcomes.