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.

Novel Inflammatory Biomarkers in Coronary Artery Disease: Potential Therapeutic Approaches.

Coronary artery disease constitutes the leading cause of mortality and morbidity in the modern world. Inflammation has been implicated to play a key role in the initiation and promotion of atherosclerosis, and the induction of plaque instability, possibly leading to acute coronary syndrome (ACS). This review aims to assess the clinical utility of well established (CRP) and novel inflammatory biomarkers (Homocyesteine, SAA, sCD40L, sLOX-1, IMA, MPO, PAPP-A and MMPs) in the diagnosis and outcome prediction of patients with ACS. The PubMed database was searched for reports using the terms "biomarkers", "acute coronary syndrome", "infarction", "markers" and only original articles written in English were included. The diversity of novel biomarkers for coronary artery disease provides an insight of the varied pathophysiology of this disease. A better understanding of their properties and assimilation in daily clinical use is essential for optimal management and patient care in the future.

Rate of percutaneous coronary intervention for the management of acute coronary syndromes and stable coronary artery disease in the United States (2007 to 2011).

Although the benefit of percutaneous coronary interventions (PCIs) for patients presenting with acute coronary syndromes (ACS) has been established in numerous studies, the role of PCI in stable coronary artery disease (CAD) remains controversial. With the publication of the Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluations trial and the appropriate use criteria for coronary artery revascularization, we sought to examine the impact of these treatment strategies and guidelines on the current practice of PCI in United States. We conducted a serial cross-sectional study with time trends of patients undergoing PCI for ACS and stable CAD from 2007 to 2011. The annual rate of all PCI decreased by 27.7% from 10,785 procedures per million adults per year in 2007 to 2008 to 7,801 procedures per million adults per year in 2010 to 2011 (p=0.03). Although there was no statistically significant decrease in the PCI utilization for ACS from 2007 to 2011, PCI utilization for stable CAD decreased by 51.7% (from 2,056 procedures per million adults per year in 2008 to 992 procedures per million adults per year in 2011, p=0.02). Hospitals with a higher volume of PCI experienced a more significant decrease. Decrease in PCI utilization for stable CAD was statistically significant for patients with Medicare and private insurance/health maintenance organization (44.5%, p=0.03 and 59.5%, p=0.007, respectively). In conclusion, the rate of PCI decreased substantially starting from 2009 in the United States. Most of the decrease was attributed to the reduction in PCI utilization for stable CAD.

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.